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IL-5-producing group 2 innate lymphoid cells promote T cell-independent IgA production in cooperation with eosinophils.
Int Immunol
December 2024
Toyama Prefectural Institute for Pharmaceutical Research, 17-1 Nakataikouyama, Imizu City, Toyama 939-0363, Japan.
Intestinal bacteria play a critical role in the regulation of the host immune system and an imbalance in intestinal bacterial composition induces various host diseases. Therefore, maintaining a balance in the intestinal bacterial composition is crucial for health. Immunoglobulin A (IgA), produced through T cell-dependent and T cell-independent (TI) pathways, is essential for host defense against pathogen invasion and maintaining the balance of intestinal symbiotic bacteria.
View Article and Find Full Text PDFThe protozoan commensal Tritrichomonas musculis is a natural adjuvant for mucosal IgA.
J Exp Med
December 2024
Department of Immunology, University of Toronto, Toronto, Canada.
Immunoglobulin (Ig) A supports mucosal immune homeostasis and host-microbiota interactions. While commensal bacteria are known for their ability to promote IgA, the role of non-bacterial commensal microbes in the induction of IgA remains elusive. Here, we demonstrate that permanent colonization with the protozoan commensal Tritrichomonas musculis (T.
View Article and Find Full Text PDFImmunoglobulin class-switch recombination: Mechanism, regulation, and related diseases.
MedComm (2020)
August 2024
Department of Pathogen Biology School of Basic Medicine, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Huazhong University of Science and Technology Wuhan Hubei China.
Maturation of the secondary antibody repertoire requires class-switch recombination (CSR), which switches IgM to other immunoglobulins (Igs), and somatic hypermutation, which promotes the production of high-affinity antibodies. Following immune response or infection within the body, activation of T cell-dependent and T cell-independent antigens triggers the activation of activation-induced cytidine deaminase, initiating the CSR process. CSR has the capacity to modify the functional properties of antibodies, thereby contributing to the adaptive immune response in the organism.
View Article and Find Full Text PDFTurbinate-homing IgA-secreting cells originate in the nasal lymphoid tissues.
Nature
August 2024
Department of Systems Immunology, Weizmann Institute of Science, Rehovot, Israel.
Nasal vaccination elicits a humoral immune response that provides protection from airborne pathogens, yet the origins and specific immune niches of antigen-specific IgA-secreting cells in the upper airways are unclear. Here we define nasal glandular acinar structures and the turbinates as immunological niches that recruit IgA-secreting plasma cells from the nasal-associated lymphoid tissues (NALTs). Using intact organ imaging, we demonstrate that nasal vaccination induces B cell expansion in the subepithelial dome of the NALT, followed by invasion into commensal-bacteria-driven chronic germinal centres in a T cell-dependent manner.
View Article and Find Full Text PDFB-cell-specific regulates microbiota composition in a primarily IgA-independent manner.
Front Immunol
January 2024
Department of Pathology, Microbiology, and Immunology, University of South Carolina School of Medicine, Columbia, SC, United States.
Background: The expression of major histocompatibility complex class II () molecules on B cells is required for the development of germinal centers (GCs) in lymphoid follicles; the primary sites for the generation of T-cell-dependent (TD) antibody responses. Peyer's patches (PPs) are secondary lymphoid tissues (SLOs) in the small intestine (SI) that give rise to high-affinity, TD antibodies (mainly immunoglobulin A (IgA)) generated against the microbiota. While several studies have demonstrated that antigen presentation by other immune cells coordinate TD IgA responses and regulate microbiota composition, whether or not B-cell-specific influences gut microbial ecology is unknown.
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