COMMON MECHANISMS OF SPECIFIC HUMORAL IMMUNE RESPONSE’ SHAPING AND SUSTAINING BY THE EXAMPLE OF IMMUNE RESPONSE TO MEASLES AND RUBELLA VIRUSES

Abstract

Abstract. T follicular helper cells (Tfh) are a CD4+ Th cell subset promoted the cognate control of antigen-specific B cell immunity. Upon first contact with antigen-primed B cells, Tfh can support either extrafollicularly differentiation into short-lived plasma cells (PC) or enter follicles to form germinal centers (GC). Signaling lymphocytic activation molecule (SLAM) interaction between Tfh and activated B-cells is essential for GC development. Within GC, Tfh regulates the fate of antigen-specific GC B cells expressing high-affinity B cell receptors to develop memory B cell (Bm) or long-lived PC. Short-lived PC produce low-affinity IgM and IgG3 early antibodies. Both Bm and long-lived PC have high-affinity class-switched IgA and IgG, predominantly IgG1 antibodies. Measles virus uses human SLAM-molecule as a cellular receptor. SLAM is expressed on dendritic cells and activated B and T-cells. This is an important regulator of the isotype switching and antibody affinity maturation, especially IgG3-IgG1 switching. Development of long-term humoral immunity, charac terized by the formation of high-affinity predominantly IgG1 antibodies, is a critical component of protective immunity to pathogens and the major goal of vaccination. However, the mechanisms involved in the shaping and sustaining of long-term humoral immunity remain poorly understood.

Keywords

• specific humoral immune response
• t follicular helper
• igg subclasses
• slam
• measles
• rubella