Innate Immunity (Biomedicine)

Autoinflammatory diseases area group of clinical conditions other than autoimmune diseases, characterized by recurrent inflammatory episodes. From apathogenetic point of view they are determined by a dys regulation of innate immunity, without involvement of specific immunity (auto reactive T cells and auto antibodies). Recently, the increased knowledge in the field of auto inflammation highlighted shared immune mechanisms in the pathogenesis of both classical monogenetic and multifactorial auto inflammatory diseases and a broad spectrum of chronic age-related inflammatory pathologies. The current increase in the prevalence of chronic inflammatory diseases makes this subject of topical interest. In the light of these considerations, we propose an update of auto inflammatory diseases and a new interpretation of auto inflammation with both theoretical and clinical implications.

The first antimicrobial peptides were isolated from the cecropia moth Hyalophora cecropia in 1980.
Since then a plethora of antimicrobial peptides have been isolated from other arthropods, invertebrates
and chordates. With the emergence of antibiotic resistant bacterial pathogens and the promising
activity of these peptides, attempts are being made to use these peptides as new antimicrobial agents.
Other researchers are interested in using these peptides to improve the resistance of crops and
livestock to infections, while another line of research is interested in using these peptides to control
vector borne diseases. Despite the promising antibacterial, antiviral, anti-protozoan and anti-tumor
activity of these peptides, relatively few peptides have made it to clinical trials. Problems associated
with the development of these peptides into effective antimicrobial agents include their higher cost,
proteolysis or decreased activity in physiological environments and mass production. This review will focus specifically on the development of insect antimicrobial peptides into useful chemotherapeutic agents.

Cationic amphiphilic peptides (CAPs) are widely studied as effectors that are activated by
microbial pathogens in immune signaling pathways of invertebrates and vertebrates. These
peptides are non-specific effectors that can kill bacteria, fungi, viruses and protozoan
parasites [1, 2]. They are a universal feature in all forms of life and are often found in all the
major barriers such as the skin and epithelia that are naturally designed for protection
against invading microorganisms. In the case of invertebrates, they play a pivotal role in
innate immunity upon which these animals depend for defense against infection. The two
immunes response strategies are interdependent and innate immunity has significant
impact on the development of adaptive immunity [3-6]. In addition to innate immunity,
vertebrates also rely on acquired immunity which is mediated by antibodies and cytotoxic T
lymphocytes [7]. Identification of these antimicrobial peptides and the study of their
structural features have led to the development of peptide drugs, sometimes through the
design of synthetic peptides based on the known structures of the natural ones. A subset of
cationic peptides has been found to have anti-tumour as well as wound-healing properties
extending the prospects of these peptides as templates for drug design strategies against
cancer and wound treatment [8]. The mechanisms by which these latter properties are
manifested are not fully understood. Indeed, the mechanisms by which cationic peptides exert their wide biological activities are still under investigation and many theories have been proposed

PURPOSE:

The normally sterile urinary tract is constantly challenged by microbial invasion leading to a high prevalence of isolated, recurrent and catheter associated urinary tract infection. The continuous emergence of bacterial resistance following overuse of traditional antibiotics requires the urgent development of alternative treatment strategies. The involvement of innate immune mechanisms in host defense is an emerging field of microbiological research with recent work focusing on the urinary tract. We performed a comprehensive literature review to establish the current level of knowledge concerning the role of innate immunity and specifically antimicrobial peptides within the human urinary tract.

MATERIALS AND METHODS:

A systematic review of the literature was performed by searching PubMed from January 1988 to September 2008. Electronic searches were limited to the English language using the key words antimicrobial, peptide and urinary. Reference lists from relevant reviews were hand searched and appropriate articles were retrieved. The proceedings of conferences held in the last 2 years by the American Urological Association, European Association of Urology and British Association of Urological Surgeons were also searched.

RESULTS:

Several defensive mechanisms have evolved in response to the threat of urinary infection, comprising physical factors and innate immune responses characterized by the expression of antimicrobial peptides. Antimicrobial peptides are small (less than 10 kDa), cationic and amphipathic peptides of variable length, sequence and structure with broad spectrum killing activity against a wide range of microorganisms including gram-positive and gram-negative bacteria. Several antimicrobial peptides have been identified in the urinary tract, and the amount and type of antimicrobial peptides expressed vary according to tissue source and disease state. These differences may reflect altered levels of innate response and, hence, susceptibility to infection. Antimicrobial peptides are already being exploited therapeutically for skin and endovascular catheter infection, and prospects for useful application in the urinary tract are emerging.

CONCLUSIONS:

Although investigation of antimicrobial peptide function in the human urinary tract is at an early stage, it is clear that there is considerable potential for the future design of novel therapeutic strategies. More knowledge is needed concerning the pathway of involvement of antimicrobial peptides in the maintenance of urinary tract sterility and the ways in which this is altered during active infection.

The use of various topical compounds for blood biting bug protection has been documented throughout written history with DEET being the current standard in chemical protection. While many minimize the danger of using DEET, it is no longer considered as completely safe to use, especially for those who are pregnant, nursing or infants. This study documents a significant change in addressing protection from haematophagous arthropods (blood seeking insects) with the use of a formulated oral solution designed to activate specific targets in the body's immunity system. By association, this reveals new and natural solutions for disrupting the pathways of disease carrying vectors. This study demonstrates and documents the efficacy of a novel biomineral complex, with a designed catalyst, that activates the human/animal created putative cloaking compounds, letting the inherent ability of the immune system create different concentrations and ratios of volatile compounds [4], to disrupt the blood seeking behavior of mosquitoes and other haematophagous arthropods. By stimulating the immune system, the body is able to protect itself instead of requiring the application of potentially harmful topical repellents. The delivery of haematophagous arthropod protection has always been problematic with the current chemical topical repellents being either toxic or very limited in their effectiveness [11] [13] [14] [15]. The NNSciences team looked at the challenge of delivering protection along a different pathway. While existing research proves that volatile vapours release semio-chemicals that create highly effective repellency [4] [5], it was limited to topical applications. The NNS team incorporated a different strategy, instead focusing on the inside of the human body, where there is already a set of NATURE NATURALLY SCIENCES All rights reserved

The immune system is based in the actions of the collection of specialized immune defense cells and their secreted proteins and peptides that defend the host against infection by parasites.  Parasites are species that live part or all of their lives in close physical association with the host and that, by extracting nutrients from the host and by the release of toxins and virulence factors, cause disease with the potential for injury and premature death of that host.  Parasites of the metazoa can be viruses, eubacteria, fungi, protozoans, and other metazoans.  The immune system operates to kill or eliminate parasites and eliminate or detoxify their toxins and virulence factors.  Although certain of the elements of immune systems are specific to a particular phylum of metazoans, others show extensive evolutionary conservation, being present in several or all major phyla of the metazoa.  The pentraxins display this latter character in their roles in immune defense.  Pentraxins have been documented in vertebrates, non-vertebrate chordates, arthropods, and mollusks and may be present in other taxa of metazoans.  Presumably the pentraxins appeared early in the evolution of the metazoa, prior to their evolutionary divergence in the Precambrian epoch into the many phyla present today, and have been preserved for the 542 million years since that explosive evolutionary radiation.  The fidelity with which these several phyla have preserved the pentraxins suggests that the functions of these proteins are important for survival of the members of these diverse taxa of animals.

The emergence of multiple-drug-resistant tuberculosis (MDR-TB) has pushed our available repertoire of anti-TB therapies to the limit of effectiveness. This has increased the urgency to develop novel treatment modalities, and inhalable microparticle (MP) formulations are a promising option to target the site of infection. We have engineered poly(lactic-co-glycolic acid) (PLGA) MPs which can carry a payload of anti-TB agents, and are successfully taken up by human alveolar macrophages. Even without a drug cargo, MPs can be potent immu-nogens; yet little is known about how they influence macrophage function in the setting of Mycobacterium tuberculosis (Mtb) infection. To address this issue we infected THP-1 mac-rophages with Mtb H37Ra or H37Rv and treated with MPs. In controlled experiments we saw a reproducible reduction in bacillary viability when THP-1 macrophages were treated with drug-free MPs. NFκB activity was increased in MP-treated macrophages, although cytokine secretion was unaltered. Confocal microscopy of immortalized murine bone marrow derived macrophages expressing GFP-tagged LC3 demonstrated induction of autop-hagy. Inhibition of caspases did not influence the MP-induced restriction of bacillary growth, however, blockade of NFκB or autophagy with pharmacological inhibitors reversed this MP effect on macrophage function. These data support harnessing inhaled PLGA MP-drug delivery systems as an immunotherapeutic in addition to serving as a vehicle for targeted drug delivery. Such " added value " could be exploited in the generation of inhaled vaccines as well as inhaled MDR-TB therapeutics when used as an adjunct to existing treatments.

Sight is one of the most important senses that human beings possess. The ocular system is a complex structure equipped with mechanisms that prevent or limit damage caused by physical, chemical, infectious and environmental factors. These mechanisms include a series of anatomical, cellular and humoral factors that have been a matter of study. The cornea is not only the most powerful and important lens of the optical system, but also, it has been involved in many other physiological and pathological processes apart from its refractive nature; the morphological and histological properties of the cornea have been thoroughly studied for the last fifty years; drawing attention in its molecular characteristics of immune response. This paper will review the anatomical and physiological aspects of the cornea, conjunctiva and lacrimal apparatus, as well as the innate immunity at the ocular surface.

The retinoblastoma binding protein 6 (RBBP6) proteins (also called P-53 Associated Cell Testis Derived
(PACT)) are highly upregulated in esophageal cancer and enhance the activity of MDM2, a p53 inhibitor
with ubiquitin ligase activity that is overexpressed in many human cancers. Mammalian RBBP6 binds
the tumour suppressor proteins p53 and the retinoblastoma protein (Rb). The invertebrate orthologues,
on the other hand, have not been shown experimentally to have these properties and they have no
obvious sequence features that are similar to the mammalian p53- and Rb-binding domains. General
features of RBBP6 proteins such as a highly conserved N-terminal ubiquitin-like domain and a RING-
finger indicate that they may be involved in proteolytic degradation of substrate proteins via the
proteasome pathway. They have recently been found to act downstream hedgehog in certain normal
developmental processes. This may implicate RBBP6 proteins in a wider range of human cancers. These data imply that antagonists of RBBP6 can be used as effective antitumour agents to treat tumours that have functional p53

Cannabis and cannabinoids offer significant therapeutic benefits for a wide scope of pathological conditions. Among them, the clinical issues rooted in inflammation stand out, nonetheless, the underlying mechanisms are not yet plainly understood. Circumstantial evidence points to polymorphonuclear leukocytes (PMN) as targets for the anti-inflammatory effects of cannabis. Therefore, we conducted this study to assess the effects of CM5, a novel Cannabis sativa L. extract standardized in 5% cannabidiol (CBD), on human PMN functions, including cell migration, oxidative metabolism and production of tumour necrosis factor (TNF)-α. We then sought to investigate whether such effects could be ascribed to its content in CBD. Cell migration was assessed by the Boyden chamber assay, oxidative metabolism by means of spectrofluorimetric measurement of reactive oxygen species (ROS) production, and TNF-α was measured by real time polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay (ELISA). Results show that both CM5 and CBD inhibit PMN migration, ROS and TNF-α production, indicating that CBD may be the main item responsible for the effects of CM5. CM5 is however more potent than CBD on cell migration and TNF-α production, and less effective on ROS production, suggesting that beyond CBD, other components of the cannabis plant may contribute to the biological effects of the extract. As a whole, such results support the use of cannabis standardized extract and CBD to stem inflammation; however, they also warrant in-depth investigation of the underlying cellular and molecular mechanisms to better exploit their therapeutic potential.

The human innate immune system defend the body against the attacks of microorganisms via different defensive protocols such as complement-mediated lysis, engulfment, constitution of neutrophil extracellular snares, and release of antimicrobial peptides (AMPs). Antimicrobial peptides are important contributors of the epithelial defensive mechanism and a number of AMPs such are defensin, cathelicidin, LL-37, LLAA etc have been described as the most important contributors. Human antimicrobial peptide LL-37 is a member of cathelicidin and is derived from granulocytes. All cathelicidin-related AMPs are family of peptides found in macrophage lysosomes and polymorphonuclear leukocytes (PMNs) and also in keratinocytes. LL-37 defence the body via its diversity of immunomodulatory functions like bactericidal action, chemotaxis, chemokine sprinkle and antisepsis affect. AMPs act as the effector molecules of innate immunity to keep the integrity of the host versus potentially adverse microorganisms safe. The antimicrobial peptides are conserved through progress and are palmate ranging from plants to mammals with hundreds of its described varieties (1, 2). ABSTRACT Antimicrobial peptides (AMPs) are the innate immune system effector molecules that serve to keep the integrity of the host versus potentially adverse microorganisms safe. Cathelicidins are a family of antimicrobial proteins organised in the peroxidase-negative neutrophil granules. The known biological actions reside in the C-terminal end and to become active it must be cleaved from the holoprotein. One of the members of this family is LL-37 which apply antimicrobial activity against both gram-positive and gram-negative bacteria and exhibit a wide spectrum antimicrobial activity versus many microorganism pathogen including viruses and fungi. LL-37 is a 37 amino acid generated polypeptide via extracellular cleavage of the C-terminus with the sequence as, NH2 LLGDFFRKSKEKIGKEFKRIVQRIKDFLRNLVPRTES-COOH and is cleaved from hCAP18 during healing of tissue cultured skin wounds to enhance innate immunity of body.

While some viruses occasionally pop-up and over-powers the
immune  system and cause deadly diseases Influenza virus is not
one among them. In contrast, Influenza infections are much
common with clinical manifestations such as common cold
however they cannot be over sighted since they can cause
uncommon consequences and even death if untreated. In this
context prevention of Influenza infection is of primordial issue.
Federal governments and pharma and biotech industries spend
billions of dollars every year to develop novel yet robust anti flu
vaccines but unfortunately we cannot shirp yet due to the fact that
the immunity offered by them is temporary thanks to their very
high rate of mutability. Currently these influenza vaccines are
produced using reassortment genetical method in embyonated
eggs. Cell culture based vaccines  have also been developed
however their efficacy is  in par  with inactivated influenza
vaccines and live attenuated influenza vaccines only. Developing a
universal influenza vaccine is the need of the hour and the future
influenza vaccines are moving in these direction. With the advent
of such universal vaccine influenza pandemics would be certainly
a past history.

Multiple sclerosis (MS) is a neurodegenerative disease of the central nervous system (CNS), traditionally considered a chronic autoimmune attack against the insulating myelin sheaths around axons. However, the exact etiology has not been identified and is likely multi-factorial. Recently, evidence has been accumulating that implies that autoimmune processes underlying MS may, in fact, be triggered by pathological processes initiated within the CNS. This review focuses on a relatively unexplored immune cell—the “innate-like” B1 lymphocyte. The B1 cell is a primary-natural-antibody- and anti-inflammatory-cytokine-producing cell present in the healthy brain. It has been recently shown that its frequency and function may differ between MS patients and healthy controls, but its exact involvement in the MS pathogenic process remains obscure. In this review, we propose that this enigmatic cell may play a more prominent role in MS pathology than ever imagined. We aim to shed light on the hu...

Multiple sclerosis (MS) is a neurodegenerative disease of the central nervous system (CNS), traditionally considered a chronic autoimmune attack against the insulating myelin sheaths around axons. However, the exact etiology has not been identified and is likely multi-factorial. Recently, evidence has been accumulating that implies that autoimmune processes underlying MS may, in fact, be triggered by pathological processes initiated within the CNS. This review focuses on a relatively unexplored immune cell—the “innate-like” B1 lymphocyte. The B1 cell is a primary-natural-antibody- and anti-inflammatory-cytokine-producing cell present in the healthy brain. It has been recently shown that its frequency and function may differ between MS patients and healthy controls, but its exact involvement in the MS pathogenic process remains obscure. In this review, we propose that this enigmatic cell may play a more prominent role in MS pathology than ever imagined. We aim to shed light on the human B1 cell in health and disease, and how dysregulation in its delicate homeostatic role could impact MS. Furthermore, novel therapeutic avenues to restore B1 cells’ beneficial functions will be proposed.

With an ever increasing number of particulate drug delivery systems being developed for the intracellular delivery of therapeutics a robust high-throughput method for studying particle-cell interactions is urgently required. Current methods used for analyzing particle-cell interaction include spectrofluorimetry, flow cytometry, and fluorescence/confocal microscopy, but these methods are not high throughput and provide only limited data on the specific number of particles delivered intracellularly to the target cell. The work herein presents an automated high-throughput method to analyze microparticulate drug delivery system (DDS) uptake byalveolar macrophages. Poly(lactic-co-glycolic acid) (PLGA) microparticles were prepared in a range of sizes using a solvent evaporation method. A human monocyte cell line (THP-1) was differentiated into macrophage like cells using phorbol 12-myristate 13-acetate (PMA), and cells were treated with microparticles for 1 h and studied using confocal laser scanning microscopy (CLSM), spectrofluorimetry and a high-content analysis (HCA). PLGA microparticles within the size range of 0.8-2.1 μm were found to be optimal for macrophage targeting (p < 0.05). Uptake studies carried out at 37 °C and 4 °C indicated that microparticles were internalized in an energy dependent manner. To improve particle uptake, a range of opsonic coatings were assessed. Coating PLGA particles with gelatin and ovalbumin was found to significantly increase particle uptake from 2.75 ± 0.98 particles per cell for particles coated with gelatin. Opsonic coating also significantly increased particle internalization into primary human alveolar macrophages (p < 0.01) with a 1.7-fold increase in uptake from 4.19 ± 0.48 for uncoated to 7.53 ± 0.88 particles per cell for coated particles. In comparison to techniques such as spectrofluorimetry and CLSM, HCA provides both qualitative and quantitative data on the influence of carrier design on cell targeting that can be gathered in a high-throughput format and therefore has great potential in the screening of intracellularly targeted DDS.

The retinoblastoma binding protein 6 (RBBP6) proteins (also called P-53 Associated Cell Testis Derived (PACT)) are highly upregulated in esophageal cancer and enhance the activity of MDM2, a p53 inhibitor with ubiquitin ligase activity that is overexpressed in many human cancers. Mammalian RBBP6 binds the tumour suppressor proteins p53 and the retinoblastoma protein (Rb). The invertebrate orthologues, on the other hand, have not been shown experimentally to have these properties and they have no obvious sequence features that are similar to the mammalian p53-and Rb-binding domains. General features of RBBP6 proteins such as a highly conserved N-terminal ubiquitin-like domain and a RING-finger indicate that they may be involved in proteolytic degradation of substrate proteins via the proteasome pathway. They have recently been found to act downstream hedgehog in certain normal developmental processes. This may implicate RBBP6 proteins in a wider range of human cancers. These data imp...

Although type 1 diabetes cannot be prevented or reversed, replacement of insulin production by transplantation of the pancreas or pancreatic islets represents a definitive solution. At present, transplantation can restore euglycemia, but this restoration is short-lived, requires islets from multiple donors, and necessitates lifelong immunosuppression. An emerging paradigm in transplantation and autoimmunity indicates that systemic inflammation contributes to tissue injury while disrupting immune tolerance. We identify multiple barriers to successful islet transplantation, each of which either contributes to the inflammatory state or is augmented by it. To optimize islet transplantation for diabetes reversal, we suggest that targeting these interacting barriers and the accompanying inflammation may represent an improved approach to achieve successful clinical islet transplantation by enhancing islet survival, regeneration or neogenesis potential, and tolerance induction. Overall, we ...

Post-translational protein deimination is mediated by peptidylarginine deiminases (PADs), which are calcium dependent enzymes conserved throughout phylogeny with physiological and pathophysiological roles. Protein deimination occurs via the conversion of protein arginine into citrulline, leading to structural and functional changes in target proteins. In a continuous series of early halibut development from 37 to 1050° d, PAD, total deiminated proteins and deiminated histone H3 showed variation in temporal and spatial detection in various organs including yolksac, muscle, skin, liver, brain, eye, spinal cord, chondrocytes, heart, intestines, kidney and pancreas throughout early ontogeny. For the first time in any species, deimination of complement components C3 and C4 is shown in halibut serum, indicating a novel mechanism of complement regulation in immune responses and homeostasis. Proteomic analysis of deiminated target proteins in halibut serum further identified complement components C5, C7, C8 C9 and C1 inhibitor, as well as various other immunogenic, metabolic, cytoskeletal and nuclear proteins. Post-translational deimination may facilitate protein moonlighting, an evolutionary conserved phenomenon, allowing one polypeptide chain to carry out various functions to meet functional requirements for diverse roles in immune defences and tissue remodelling.

C1q is the first subcomponent of the classical complement pathway that binds antigen-bound IgG or IgM and initiates complement activation via association of serine proteases C1r and C1s. The globular domain of C1q (gC1q), which is the ligand-recognition domain, is a heterotrimeric structure composed of the C-terminal regions of A (ghA), B (ghB), and C (ghC) chains. The expression and functional characterization of ghA, ghB, and ghC modules have revealed that each chain has some structural and functional autonomy. Although a number of studies have tried to identify IgG-binding sites on the gC1q domain, no such attempt has been made to localize IgM-binding site. On the basis of the information available via the gC1q crystal structure, molecular modeling, mutational studies, and bioinformatics, we have generated a series of substitution mutants of ghA, ghB, and ghC and examined their interactions with IgM. The comparative analysis of IgM- and IgG-binding abilities of the mutants suggests that the IgG- and IgM-binding sites within the gC1q domain are different but may overlap. Whereas Arg(B108), Arg (B109), and Tyr(B175) mainly constitute the IgM-binding site, the residues Arg(B114), Arg(B129), Arg(B163), and His(B117) that have been shown to be central to IgG binding are not important for the C1q-IgM interaction. Given the location of Arg(B108), Arg (B109), and Tyr(B175) in the gC1q crystal structure, it is likely that C1q interacts with IgM via the top of the gC1q domain.

C1q is the first subcomponent of the classical complement pathway that binds antigen-bound
IgG or IgM and initiates complement activation via association of serine proteases C1r and C1s. The
globular domain of C1q (gC1q), which is the ligand-recognition domain, is a heterotrimeric structure
composed of the C-terminal regions of A (ghA), B (ghB), and C (ghC) chains. The expression and functional
characterization of ghA, ghB, and ghC modules have revealed that each chain has some structural and
functional autonomy. Although a number of studies have tried to identify IgG-binding sites on the gC1q
domain, no such attempt has been made to localize IgM-binding site. On the basis of the information
available via the gC1q crystal structure, molecular modeling, mutational studies, and bioinformatics, we
have generated a series of substitution mutants of ghA, ghB, and ghC and examined their interactions
with IgM. The comparative analysis of IgM- and IgG-binding abilities of the mutants suggests that the
IgG- and IgM-binding sites within the gC1q domain are different but may overlap. Whereas ArgB108, Arg
B109, and TyrB175 mainly constitute the IgM-binding site, the residues ArgB114, ArgB129, ArgB163, and HisB117
that have been shown to be central to IgG binding are not important for the C1q-IgM interaction. Given
the location of ArgB108, Arg B109, and TyrB175 in the gC1q crystal structure, it is likely that C1q interacts
with IgM via the top of the gC1q domain.

C1q, the recognition subunit of the classical complement pathway, is a multifunctional
protein involved in a great number of immunological processes. The molecular basis of
the functional diversity of C1q is its ability to recognize a broad range of ligands via the
gC1q region. One of the most important ligands of C1q is the human C-reactive protein
(CRP), a major acute phase protein, which plays a crucial role in keeping the tolerance to
self-structures. The aim of the present study is to evaluate the contribution of the C1q
globular head fragments rghA, rghB and rghC to the recognition of CRP. The obtained
results indicate that all three C1q-chains are involved in the CRP-binding, and that rghB
is the most important one. The pH-dependence of the interactions between rghA/B/C and
CRP demonstrates that different amino acid residues from the three chains take part in the
formation of the CRP-binding site. The analysis of the CRP-binding activities of biotinylated
and nonbiotinylated rghB indicates that Tyr residues from the ghB are the most
likely to play a crucial role in the interaction with CRP and that probably only one Lys
residue from the rghB is involved as well.

Antimicrobial peptides (AMPs) are activated in response to septic injury and have important roles in vertebrate and invertebrate
immune systems. AMPs act directly against pathogens and have both wound healing and antitumor activities. Although
coleopterans comprise the largest and most diverse order of eukaryotes and occupy an earlier branch than Drosophila in the
holometabolouslineageofinsects,theirimmunesystemhasnotbeenstudiedextensively.Initialresearchreports,however,indicate
that coleopterans possess unique immune response mechanisms, and studies of these novel mechanisms may help to further
elucidate innate immunity. Recently, the complete genome sequence of Tribolium was published, boosting research on coleopteran
immunity and leading to the identification of Tribolium AMPs that are shared by Drosophila and mammals, as well as other
AMPs that are unique. AMPs have potential applicability in the development of vaccines. Here, we review coleopteran AMPs, their
potential impact on clinical medicine, and the molecular basis of immune defense.