TCR gamma delta cells: a specialized T-cell subset in the immune system.
Specificity, memory, and self/nonself discrimination are the essential principles that underlie the acquired immune response. From birth through one's life, the immune system is continually responding to new environmental challenges (e.g. bacteria and viruses) and developing a specific, long-lasting immunity to those challenges. The first exposure to a pathogen results in the recruitment of multiple cell types, including macrophages, dendritic cells, and assorted leukocytes, that initiate an antigen nonspecific inflammatory response designed to attract T cells and B cells to the inflammatory sites including the draining lymph nodes. The foreign antigens are concentrated within the professional antigen-presenting cells (APCs) that process and present small antigenic peptides to CD4+ and CD8+ T cells in association with class II and class I major histocompatibility complex (MHC) molecules, respectively. The activated CD4+ T-cell receptor (TCR) alpha beta cells respond vigorously to the pathogen in an antigen-specific manner, liberating a barrage of cytokines that induce B cells to differentiate to antibody-secreting plasma cells and likewise cause CD8+ cells to differentiate into cytolytic effectors. The T cells and B cells expand in an evolving, highly specific manner to control the initial infection while developing long-term acquired immunity such that any further infection by that pathogen is virtually impossible. Thus TCR alpha beta T cells are the central lymphocyte in the immune system, providing specific pathogen recognition and long-term memory all within the context of distinguishing foreign from self antigens. Yet, during a primary immune response, there is a lag time of approximately 3 to 4 days before antigen-specific responses are evident, and TCR alpha beta responses do not peak until approximately day 7. Therefore, it is essential that other strategies are employed by the immune system in order to mount an aggressive early immune response.
Bluestone
J A
JA
University of Chicago, Ben May Institute, Illinois, USA.
Khattri
R
R
Sciammas
R
R
Sperling
A I
AI
D000818:Animals; D001402:B-Lymphocytes / Q000276:immunology; D018106:CD28 Antigens / Q000276:immunology; D006681:HLA-D Antigens / Q000276:immunology; D006360:Heat-Shock Proteins / Q000276:immunology; D015395:Histocompatibility Antigens Class I / Q000276:immunology; D000949:Histocompatibility Antigens Class II / Q000276:immunology; D006801:Humans; D007109:Immunity; D007156:Immunologic Memory; D007249:Inflammation; D008222:Lymphokines / Q000276:immunology; D008285:Major Histocompatibility Complex; D016692:Receptors, Antigen, T-Cell, gamma-delta / Q000276:immunology*; D015398:Signal Transduction; D013379:Substrate Specificity; D016176:T-Lymphocyte Subsets / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology
D018106:CD28 Antigens; D006681:HLA-D Antigens; D006360:Heat-Shock Proteins; D015395:Histocompatibility Antigens Class I; D000949:Histocompatibility Antigens Class II; D008222:Lymphokines; D016692:Receptors, Antigen, T-Cell, gamma-delta