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PubMedDate not supplied

Defensins: natural anti-HIV peptides.

Mammalian defensins are small cationic antimicrobial peptides predominantly found in leukocytes and epithelial cells engaged in host defense. These peptides act as effector molecules in innate immunity as well as regulators in adaptive immunity. Increasing evidence indicates that defensins are effective inhibitors of HIV-1. While the level of defensins in HIV-1 infected individuals has not been determined, neutropenia and neutrophil dysfunction associated with HIV disease progression may result in altered alpha-defensin production. This review provides an overview of the structure and function of defensins, and focuses on the anti-HIV-1 activity of defensins and the mechanism of this activity. Although many questions remain, studying the complex function of defensins in innate immunity against HIV has implications for our further understanding of disease progression and for the development of novel approaches to prevention and therapy.

Amino Acid Sequence↗

PubMed2004

Toll-like receptors involved in the response to microbial pathogens: development of agonists for toll-like receptor 9.

Upon microbial infection, a host has to mount a multiplicity of immune responses that target the invading pathogen. This is achieved in part by the use of particular receptors expressed on mammalian innate immune cells, the toll-like receptors (TLRs). Recognition of a given microbial molecular structure, such as bacterial or viral DNA, leads to the activation of signaling pathways that result in distinct sets of immune responses. The pathogen structures that are recognized by TLR9 in bacterial or viral DNA are deoxycytidyl-deoxyguanosine dinucleotides (CpGs) in specific sequence contexts (CpG motifs). The stimulatory activity of pathogen DNA can be mimicked by synthetic oligodeoxynucleotides (ODNs) containing such motifs (CpG ODNs). The TLR9-mediated stimulation of the vertebrate innate immune system, and subsequently of the adaptive immune system, allows the use of TLR9 agonists as highly effective vaccine adjuvants for infectious diseases, and as stand-alone therapies or in combination with other therapies in cancer.

Adjuvants, Immunologic↗

PubMed2005

The potential immunomodulatory effects of topical retinoids.

New research has refined our understanding of the immunopathophysiology of acne. Various immune factors, including both innate and adaptive immune responses, have been implicated in the pathophysiology of inflammatory acne. Topical retinoids such as tretinoin, adapalene, and tazarotene, exhibit immunomodulatory effects that may help to explain their efficacy in the resolution of inflammatory lesions.

Acne Vulgaris↗

PubMed2005

[Understanding rheumatoid arthritis].

Rheumatoid arthritis is a common and severe inflammatory rheumatic disease, for which the immune mechanisms are being decoded little by little. The pathogenic ncludes significant cellular actors of innate immunity (fibroblastic synoviocytes, macrophages, mastocytes...) and adaptive immunity (T and B lymphocytes). These actors interact through the production of and response to specific (cytokines, chemokines and auto-antibodies) and non-specific (prostaglandins, nitrous oxide [NO], complement, proteases) mediators. The chronology of this rheumatoid synovitis is becoming progressively clearer. Its initiation could be the consequence of a precocious activation of the innate immunity, induced by bacterial agents or debris (PAMP). The activation of the synoviocytes and the macrophages via specific receptors (PPR) unleashes an intense inflammatory reaction that triggers a cascade of events. The ongoing nature of this synovitis leads to the intra-articular recruitment of different cells of immunity. This cellular afflux amplifies the macrophagic and synoviocytic activation and proliferation. All of these interactive phenomena end in the production of large quantities of pro-inflammatory cytokines (TNFa, IL1, IL6, IL15, IL17, IL18) but also other pathogenic mediators (auto-antibodies, complement, prostaglandins, nitrous oxide...). This synovitis persists, as it is no longer regulated by a sufficient production of physiological regulators (soluble receptors and inhibitors of cytokines). The consequence of this intense inflammation and synovial proliferation leads to osteo-articular destruction by the production of proteases and the activation of osteoclasts by the RANK/RANK-ligand pathway under the effect of cytokines (TNFa, IL5, IL1, IL6, IL17) and other mediators (prostaglandins) liberated by synoviocytes, macrophages and lymphocytes. The decryption of this puzzle has already created new therapeutic orientations. The identification of new targets is one of the major consequences of this progress in immuno-rheumatology.

Arthritis, Rheumatoid↗

PubMed2006

Infection with Porcine reproductive and respiratory syndrome virus stimulates an early gamma interferon response in the serum of pigs.

The early release of cytokines by cells involved in innate immunity is an important host response to intracellular pathogens. Gamma interferon (IFN-gamma) is an important cytokine produced during the early stages of an infection by macrophages, natural killer (NK) cells, and other cell types, and it is also a central cytokine mediator for the induction of cellular or Th1 immunity. To better understand innate and adaptive immune responses after infection with Porcine reproductive and respiratory syndrome virus (PRRSV), we investigated serum IFN-gamma concentrations and the duration of viremia. For 2 strains of atypical PRRSV, IFN-gamma was detectable in swine serum soon after infection and lasted for approximately 3 wk. Serum concentrations of IFN-gamma peaked at about 10 d after inoculation and returned to approximately baseline levels by day 22. However, individual pigs manifested short, sporadic increases in the serum concentration of IFN-gamma from 18 to 50 d after inoculation. Prior vaccination blocked the serum IFN-gamma response associated with homologous virus challenge and altered the kinetics of the response after heterologous challenge. Two other respiratory viruses of pigs, Porcine respiratory coronavirus and Swine influenza virus, do not appear to induce serum IFN-gamma. The early production of IFN-gamma in PRRSV-infected pigs might result from activation of NK cells, a response that is more characteristic of immune pathways stimulated by intracellular bacterial and protozoan infections.

Animals↗

PubMed2006

The role of cytokines in the immune response to influenza A virus infection.

Influenza A virus is one of the most important causes of respiratory tract diseases. It replicates in epithelial cells and leukocytes resulting in the production of immune mediators--cytokines, substances with various biological effects. Cytokines, as a part of innate immunity, favor the development of antiviral and TH 1-type immune responses. Cytokines also affect the adaptive immune response and disease manifestation. In the organism, the virus infection results in the production of chemotactic [a regulated upon activation, normal T cell-expressed and -secreted cytokine (RANTES), monocyte chemoattractant proteins (MCP) MCP-1, MCP-3, macrophage inflammatory protein 1 alpha (MIP- 1 alpha), interferon gamma-induced protein 10 (IP-10), and interleukin 8 (IL-8)], pro-inflammatory [IL- 1beta, IL-6, IL-18, and tumor necrosis factor alpha(TNF-alpha)] and antiviral [interferon (IFN) alpha/beta] cytokines. Whilst knowledge of the mechanisms underlying host and tissue specificity has advanced significantly, we still know relatively little about the function of cytokines released from different cells following influenza infection. In this review we deal with the role and mode of possible impact of cytokines on the disease pathogenesis and host immune response.

Animals↗

PubMed2006

FcgammaRII and multi-system autoimmune disease.

The FcR are a crucial link in the immune response between humoral and cellular immunity and cell-based effector systems, mediating a wide variety of physiological and biochemical responses. The FcR for IgG (FcgammaR) and in particular the most widely expressed of these, FcgammaRII, are important in regulating adaptive immunity. Disruption of their function is a key factor in the development of autoimmune diseases such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA), which are characterized by chronic, multi-organ inflammation. Studies of the FcgammaRII include structure/function relationships, investigation of the associations between FcR polymorphisms and human disease and animal studies using knockout or transgenic mouse models. These investigations showed that the various forms of FcgammaRII interact with immune complexes to either initiate or inhibit inflammation. In conjunction with environmental antigens and genotype, the FcgammaRII activating and inhibitory receptors determine the nature and magnitude of response to antigens. In this review, the structure and function of the FcgammaRIIs and their role in immune complex-mediated auto-immunity are discussed.

Adaptive Immunity↗

PubMed2004

Pneumonia caused by Mycobacterium kansasii in a series of patients without recognised immune defect.

The clinical and epidemiological characteristics of 17 patients diagnosed with Mycobacterium kansasii pneumonia within a limited geographical region over a period of 10 years are described. An in-depth evaluation of the innate and adaptive immune systems was performed for five available patients. A comparison was made of the genetic fingerprint patterns of the isolates obtained by restriction fragment length polymorphism (RFLP) analysis, with the major polymorphic tandem repeat (MPTR) as a probe. Predisposing factors consisted of smoking, airway abnormalities, substance abuse, diabetes or poor general condition, but in two patients no risk factor was identified. In the five patients tested, no abnormalities or deficiencies were detected in the innate or adaptive type-1 immunity. All M. kansasii isolates had identical MPTR RFLP patterns, although no epidemiological connection could be established, and these were identical to those of clinical isolates from Australian patients. These data do not support the theory that defects in the innate or adaptive type-1 immunity have a role in the pathogenesis of invasive M. kansasii infections. The identical fingerprint patterns of the isolates suggested the existence of a virulent strain of M. kansasii.

Adult↗

PubMed2006

The CARMA1 signalosome links the signalling machinery of adaptive and innate immunity in lymphocytes.

The recognition of antigen by B- or T-cell receptors initiates an intracellular signalling cascade that results in the nuclear translocation and activation of the transcription factor nuclear factor-kappaB (NF-kappaB). NF-kappaB is an important regulator of lymphocyte development and function, and its dysregulation is associated with many immune disorders. Defining the mechanisms that transmit signals from the antigen receptor to NF-kappaB is therefore an important goal for immunologists. In this Review, we merge information gleaned from research of the innate immune system with what we know about antigen-receptor signals in the adaptive immune system, to propose a cohesive model of how antigen receptors activate NF-kappaB.

Animals↗

PubMed2006

Cutting Edge: Plasmacytoid dendritic cells provide innate immune protection against mucosal viral infection in situ.

Dendritic cells (DCs) are powerful APCs capable of activating naive lymphocytes. Of the DC subfamilies, plasmacytoid DCs (pDCs) are unique in that they secrete high levels of type I IFNs in response to viruses but their role in inducing adaptive immunity remains divisive. In this study, we examined the importance of pDCs and their ability to recognize a virus through TLR9 in immunity against genital HSV-2 infection. We show that a low number of pDCs survey the vaginal mucosa at steady state. Upon infection, pDCs are recruited to the vagina and produce large amounts of type I IFNs in a TLR9-dependent manner and suppress local viral replication. Although pDCs are critical in innate defense against genital herpes challenge, adaptive Th1 immunity developed normally in the absence of pDCs. Thus, by way of migrating directly into the peripheral mucosa, pDCs act strictly as innate antiviral effector cells against mucosal viral infection in situ.

Animals↗

PubMed1989

Immunotoxicology: suppressive and stimulatory effects of drugs and environmental chemicals on the immune system. A discussion.

The fundamental characteristic of the adaptive immune system which has evolved in the vertebrates is the ability to recognise, and subsequently destroy, "foreign", and potentially harmful, antigens. The selective advantage which the immune system confers is the capacity to resist infectious, and possibly malignant, disease. It has been apparent for many years that individuals in whom immune function is impaired, due either to a congenital defect or to other factors such as treatment with certain immunosuppressive drugs, exhibit an increased susceptibility to infection and, in some cases, an elevated risk of developing at least some forms of malignancy. There is an increasing awareness from rodent studies that a variety of drugs and environmental chemicals have the potential to unintentionally impair components of the immune system. Risk assessment, based upon data from chemically induced changes in one or more parameters of immune function, is, however, dependent upon a knowledge of the functional reserve of the immune system. One of the objectives of the meeting from which this report derives was to examine what sources of information are available, and what experimental protocols can be employed, to permit accurate evaluation of immunological reserve. Although, under normal circumstances, the immune system selectively and specifically recognises foreign antigen, it is clear that the potential to recognise "self" is present and that in certain circumstances this potential is realised. Antibodies directed against normal tissue antigens have been shown to be associated with, and in some instances the presumptive cause of, "autoimmune" disease. There is a growing list of drugs and chemicals which are capable of eliciting autoantibodies and pathological autoimmune reactions. A second purpose of this meeting and of this report was to review the current state of knowledge regarding drug- and chemical-induced autoimmunity.

Adjuvants, Immunologic↗

PubMed2003

Autoimmunity as a special case of immunity: removing threats from within.

The function of the adaptive immune response against exogenous (non-self) agents is to help the innate arm of the immune system (represented by phagocytic cells) to fight and eliminate these agents. We suggest that the body also protects itself against potentially harmful self components using mechanisms similar to those used for fighting and eliminating non-self agents, and that the protective immune activity against self-components competes with the activity of self-destructive compounds. Tolerance to self is thus not a lack of response to self, but the ability to tolerate an active defense response to self without developing an autoimmune disease.

Autoimmune Diseases↗

PubMed2005

Are innate immune signaling pathways in plants and animals conserved?

Although adaptive immunity is unique to vertebrates, the innate immune response seems to have ancient origins. Common features of innate immunity in vertebrates, invertebrate animals and plants include defined receptors for microbe-associated molecules, conserved mitogen-associated protein kinase signaling cascades and the production of antimicrobial peptides. It is commonly reported that these similarities in innate immunity represent a process of divergent evolution from an ancient unicellular eukaryote that pre-dated the divergence of the plant and animal kingdoms. However, at present, data suggest that the seemingly analogous regulatory modules used in plant and animal innate immunity are a consequence of convergent evolution and reflect inherent constraints on how an innate immune system can be constructed.

Adaptor Proteins, Vesicular Transport↗

PubMedDate not supplied

Immune responses: adverse versus non-adverse effects.

The adaptive immune system in vertebrates has evolved to provide host resistance to infectious microorganisms and malignant disease. Normal immune function and the induction of specific immune responses require the orchestrated interaction between cells and molecules both within and outside the lymphoid system. Immunotoxicology can be defined as the study of adverse health effects that may result from the interaction of xenobiotics with the immune system. In general terms such effects can take one of two forms. The first of these is immunotoxicity (or immunosuppression) where there is a perturbation of, or damage to, one or more components of the immune system resulting in impaired immune function and reduced host resistance. The design and interpretation of experimental immunotoxicity studies and the investigation of clinical immunosuppression require consideration of the relationship between changes in the structure and/or function of discrete components of the immune system and holistic changes in the susceptibility to infectious and malignant disease. The other main way in which chemicals may cause adverse health effects secondary to interaction with the immune system is through stimulation of specific immune responses that result in allergic disease. Allergy to chemicals and proteins can take many forms, including allergic contact dermatitis, allergic sensitization of the respiratory tract (associated with rhinitis and/or asthma), systemic allergic reactions (associated frequently with drug treatment), and gastrointestinal disease. Here there is a need to distinguish between immunogenic responses per se and those immune responses that are of sufficient vigor and of the quality necessary to provoke allergic sensitization. The purpose of this article is to explore the extent to which distinctions can be drawn between adverse and nonadverse effects in the context of immunotoxicity and allergy.

Animals↗

PubMed2000

In situ analysis of the evolution of the primary immune response in murine Chlamydia trachomatis genital tract infection.

Adaptive immune responses contribute to the resolution of Chlamydia trachomatis genital tract infection and protect against reinfection, but our understanding of the mechanisms of those protective responses is incomplete. In this study, we analyzed by in situ immunohistochemistry the progression of the inflammatory and cytokine responses in the genital tracts of mice vaginally infected with C. trachomatis strain mouse pneumonitis. The cellular inflammatory response was characterized by an initial elevation in myeloid cells in the vagina (day 3) and uterine horns (day 7), followed by a marked rise in the number of T cells, predominantly CD4(+) cells. CD8(+) T cells and CD45R(+) B cells were also detected but were much less numerous. Perivascular clusters of CD4(+) T cells, which resembled clusters of T cells seen in delayed-type hypersensitivity responses, were evident by 2 weeks postinfection. Following the resolution of infection, few CD8(+) T cells and CD45R(+) B cells remained, whereas numerous CD4(+) T cells and perivascular clusters of CD4(+) T cells persisted in genital tract tissues. Interleukin-12 (IL-12)- and tumor necrosis factor alpha (TNF-alpha)-producing cells were observed in vaginal tissue by day 3 of infection and in uterine tissues by day 7. Cells producing IL-4 or IL-10 were absent from vaginal tissues at day 3 of infection but were present in uterine tissues by day 7 and were consistently more numerous than IL-12- and TNF-alpha-producing cells. Thus, the evolution of the local inflammatory response was characterized by the accumulation of CD4(+) T cells into perivascular clusters and the presence of cells secreting both Th1- and Th2-type cytokines. The persistence of CD4(+)-T-cell clusters long after infection had resolved (day 70) may provide for a readily mobilizable T-cell response by which previously infected animals can quickly respond to and control a secondary infectious challenge.

Animals↗

PubMed2025

Prior vaccination prevents overactivation of innate immune responses during COVID-19 breakthrough infection.

At this stage in the COVID-19 pandemic, most infections are "breakthrough" infections that occur in individuals with prior severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) exposure. To refine long-term vaccine strategies against emerging variants, we examined both innate and adaptive immunity in breakthrough infections. We performed single-cell transcriptomic, proteomic, and functional profiling of primary and breakthrough infections to compare immune responses from unvaccinated and vaccinated individuals during the SARS-CoV-2 Delta wave. Breakthrough infections were characterized by a less activated transcriptomic profile in monocytes and natural killer cells, with induction of pathways limiting monocyte migratory potential and natural killer cell proliferation. Furthermore, we observed a female-specific increase in transcriptomic and proteomic activation of multiple innate immune cell subsets during breakthrough infections. These insights suggest that prior SARS-CoV-2 vaccination prevents overactivation of innate immune responses during breakthrough infections with discernible sex-specific patterns and underscore the potential of harnessing vaccines in mitigating pathologic immune responses resulting from overactivation.

Immunity, Innate↗

PubMed2026

T Cell Thoughts.

This review does not aspire to provide comprehensive coverage of any particular area. Rather, it is an attempt to reconsider and summarize the results produced by our team in the field of TCR repertoires over the past 15 years, and to correct some of the errors along the way. As intended, it is unavoidably subjective, one-sided, and full of citations to the author's publications. Nevertheless, I hope it will be useful to the immunological community. Someone, having read this relatively short text, will realize that there is no need to spend time studying our previous publications. And one might discover the only useful point of our collective effort hidden in a Supplementary Figure X of a previously unnoticed publication Y. The key points are formulated below as a set of short chapters. Their order does not follow the chronology of the cited works and only intermittently resembles a coherent narrative. In an attempt to summarize, we will speak here about the TCR repertoire preferences of T cell subsets, the plasticity and stubbornness of clonal memory, the price we pay for the privilege of possessing adaptive immunity, some secrets of healthy longevity, about repertoire-based diagnostics, and about immunotherapeutic approaches considered as a toolbox for correcting mistakes made by the immune system.

Humans↗

PubMed2004

IL-5 links adaptive and natural immunity in reducing atherosclerotic disease.

Oxidized LDL induces changes in several facets of the immune system, although the relationships between these facets and their contributions to atherogenesis have yet to be fully elucidated. A report in this issue of the JCI provides a novel demonstration of the adaptive immune system influencing the production of natural antibodies. The results demonstrate that injection of malondialdehyde-modified LDL promotes a Th2 response that in turn increases the titers of the natural antibody T15/EO6, which recognizes the oxidized phospholipid POVPC. Atherosclerotic lesion size in LDL receptor-deficient mice is reduced as a consequence of the increase in natural antibody titers, and IL-5 is identified as the link between the adaptive and natural immune systems.

Animals↗