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. Author manuscript; available in PMC: 2015 Dec 1.
Published in final edited form as: Semin Immunol. 2014 Oct 28;26(6):588–600. doi: 10.1016/j.smim.2014.10.005

Figure 1. Mechanisms by which B cells shape the immune response to M. tuberculosis.

Figure 1

B cells could regulate the host response to M. tuberculosis by: 1) functioning as antigen presenting cells to interact with T cells: the primary site of this reaction is at the germinal center (GC). The interaction between GC B cells and Tfh (T follicular helper cells) culminates in B cell expansion, somatic hypermutation, affinity maturation, class switching, and the development of memory B cells and antibody-producing plasma cells; 2) producing cytokines that modulate responding immune cells including influencing the differentiation of T cells and hence effector functions; and 3) producing antibodies (Ab) which could modulate multiple aspects of both the innate and adaptive immune response. M. tuberculosis-specific antibodies can opsonize extracellular bacilli, form immune complex that fix complements, and engage Fcγ receptors of effector cells thereby modulating their functions and therefore, their effects on other immune cells, including T cells. Antibodies can also modulate the GC reactions as we as inflammation in infected tissues. LT: lymphotoxin; TGF: transforming growth factor; IL: interleukin; TNF: tumor necrosis factor; APC: antigen presenting cell; GC: germinal center; Ab: antibodies; Red oval: M. tuberculosis antigen; Pink circles: secreted cytokines; Green Y: IgG; Pink double Y: dimeric IgA; Blue snowflake: pentameric IgM; Maroon double Y: B cell receptor.