Pathogenesis of Fungal Keratitis
Mahendra Rai, Marcelo Luís Occhiutto in Mycotic Keratitis, 2019
Physiological host defense apparatus is abundant and sophisticated, developed as a biologic evolutionary defense strategy against microorganisms, which is called “innate immunity” or “innate immune system”. The innate immune system are responsible for recruiting immune cells, activate the complement cascade, and evoke the adaptive immune system through a physiological process known as antigen presentation. The adaptive immune system is a very refined set of mechanisms composed of highly specific cells directed to eliminate pathogens or prevent their installation and growth, as well as responsible to create immunological memory after an initial response. Both mechanisms are present and active in the occurrence of a fungal infection, but they are not enough to restrain tissue invasion and its destruction caused by fungi.
Dermal Hypersensitivity: Immunologic Principles and Current Methods of Assessment
David W. Hobson in Dermal and Ocular Toxicology, 2020
The primary role of the immune system is defense of the host against disease. Immunity involves both innate and adaptive mechanisms (Table 1). The epithelial surfaces of the body serve as major nonspecific barriers to infections, in the structural form of external skin and internal mucous membranes. Components within these structures also play a major role in adaptive resistance to disease. Adaptive immunity manifests the ability to distinguish between self and nonself antigens and to mount a specific host-defense response against foreign molecules. The adaptive immune system consists of a complex network of immunocytes (primarily lymphocytes and macrophages) and regulatory cytokines (soluble biomolecules secreted from cells) which act in unison to generate an immune response.24 Activation of this system requires antigen presentation by macrophages, and differentiation and clonal proliferation of lymphocytes (Figure 1).
Immunoglobulin E: Pathogenic Relevance in Urticaria and Eczema
Ana M. Giménez-Arnau, Howard I. Maibach in Contact Urticaria Syndrome, 2014
The innate immune system is characterized as generating a quick response after its encounter with the pathogen (antigen or allergen), whereas the adaptive immune system has a specialized response, amplifying it after repeated exposures to the same pathogen. During development, T-cell lymphocyte maturation is mediated by cytokines and cell–cell interaction. There are two important types of T-cell lymphocytes regarding cell-surface markers: 1) CD4+, also called helper T cells (Th) (60%–70%) and 2) CD8+, also called suppressor T cells (30%–40%). Depending on the type of cytokine produced, Th cells differentiate into type 1 (Th1), type 2 (Th2), and the newly identified subsets, Th17 and Th22.[1,2] Whereas interleukins (IL) 4 and 13 are cytokines that induce a Th2 balance, IL-2 and interferon-γ (IFN-γ) induce Th1 environment. Th2 cells stimulate immunoglobulin (Ig) E production by B cells. The balance of these stimulatory and inhibitory activities of the Th1 and Th2 is believed to determine an individual’s propensity to develop allergic disorders or atopy. The predominance of Th1 or Th2 response in each individual has been demonstrated to be influenced by environmental factors as well as by genetic predisposition by particular population.[3] In fact, children from allergic parents are more susceptible to develop allergic disorders.[4,5] On the other hand, Th17 and Th22 cells have been described in the context of asthma, where the neutrophil is predominant in the infiltrate, and in non-IgE-related atopic eczema as well as in chronic phases of atopic eczema.[2,6]
Immunologic evaluation and genetic defects of apoptosis in patients with autoimmune lymphoproliferative syndrome (ALPS)
Published in Critical Reviews in Clinical Laboratory Sciences, 2021
Laura Casamayor-Polo, Marta López-Nevado, Estela Paz-Artal, Alberto Anel, Frederic Rieux-Laucat, Luis M. Allende
The adaptive immune system plays a crucial role in defending the organism against pathogens. After initiation of the immune response, lymphocytes proliferate and differentiate into effector cells. The expansion phase is needed to generate enough effector T cells specific for the pathogen. Finally, antigen-activated lymphocytes require an effective control of their life span to maintain lymphocyte homeostasis. Apoptosis reduces lymphocyte numbers during the contraction phase of an immune response. During the shut-down of the immune response, activated lymphocytes are removed by two mechanisms: T cells that are restimulated toward the end of the immune response die by AICD, and activated lymphocytes that are not restimulated die by activated cell autonomous death [127]. AICD is shown to be partially impaired in patients with ALPS-FASLG [60–62]. These reports highlight the usefulness of AICD combined with a Fas-induced apoptosis assay to discriminate cases of ALPS-FAS and ALPS-FASLG. The mechanism consists of reactivation of previously in vitro-activated lymphocytes to induce the expression of FasL, which will trigger apoptosis by AICD.
CRISPR/Cas: from adaptive immune system in prokaryotes to therapeutic weapon against immune-related diseases
Published in International Reviews of Immunology, 2020
Juan Esteban Garcia-Robledo, María Claudia Barrera, Gabriel J. Tobón
All organisms are part of the three main branches of the tree of life, bacteria, archaea (prokaryotes), and eukaryotes, that split from a common Last Universal Common Ancestor (LUCA) [2, 15]. Multicellular eukaryotes comprising most of kingdom Animalia emerged approximately 600 million years ago during the metazoan age [16]. These metazoan organisms branched rapidly along different lineages, and about 500 million years ago multiple lineages emerged [16]. Even simple life forms such as prokaryotes and single-celled eukaryotes possess heritable innate immune mechanisms [17]. Alternatively, adaptive immune systems able to provide protection based on previous exposure to foreign invaders was thought to first appear with the rise of jawed vertebrates (a metazoan lineage) [16, 18]. The adaptive immune system is based on cellular and humoral components (T cells and B lymphocytes, respectively) expressing antigen-recognizing receptors. These receptors are formed by genetic recombination during cell fate determination and maturation, allowing for the creation of multiple cell clones expressing receptors specific for different epitopes of microorganisms [18, 19].
Inflammatory B cells correlate with failure to checkpoint blockade in melanoma patients
Published in OncoImmunology, 2021
Kaat de Jonge, Laure Tillé, Joao Lourenco, Hélène Maby-El Hajjami, Sina Nassiri, Julien Racle, David Gfeller, Mauro Delorenzi, Grégory Verdeil, Petra Baumgaertner, Daniel E. Speiser
B cells make up an important part of the adaptive immune system. Their role and function in the immune response to cancer still remain unclear. We found that circulating B cells from melanoma patients are often functional, as they produce GMCSF, IL-2, IL-6, TNFα, LTα and IL-10. Furthermore, we observed a correlation between treatment failure to anti-CTLA4 therapy and inflammatory circulating B cells, and inverse correlations of B cells producing IL-6 and TNFα with overall patient survival. IL-6 is able to inhibit apoptosis in cancer cells as well as to induce angiogenesis. Its presence, as also measured in sera, is often associated with progression in melanoma .44 IL-6 also induces the transcription factor c-Maf in T cells which promotes CD4 Th17 cells and CD8 T cell exhaustion .45,46 TNFα induces immune-regulatory genes in melanoma .47 Even though TNFα is able to induce apoptosis in tumor cells, prolonged exposure may induce survival molecules like anti-apoptotic proteins, proangiogenic factors and metastasis markers .48
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