TB, or not TB: that is the question – does TLR signaling hold the answer?
J. Clin. Invest. Terence M. Doherty, et al. 114:1699 doi:10.1172/JCI23867 [Go to this article.]

Figure 2
Bridge between innate and adaptive immunity. MTB is incorporated into phagosomes (P) of APCs by one of several receptors, which appear to have a unique impact on subsequent signaling by mechanisms that are not yet clear. TLR-dependent signaling is stimulated by association of TLRs with pathogen-associated molecular patterns located on the cell surface as well as in the phagosomes. Antigenic fragments are processed and presented by MHC class II molecules to T cells, which can then be activated provided they receive appropriate costimulatory signals transduced by engagement of T cell receptors (CD28 and CTLA-4) by CD80 (B7.1) or CD86 (B7.2) that are expressed by APCs. Normal TLR-MyD88 signaling results in rapid and potent upregulation of Th1 cytokines, which are essential for effective innate immune defense but also have a profound impact on subsequent adaptive immunity via their effects on T cell activation and maturation. Activated T cells and NK cells express IFN-γ, which stimulates activated APCs to continue to produce Th1 cytokines. However, in the absence of MyD88, expression of Th1 cytokines is markedly compromised, and Th2 cytokines may then predominate and inappropriately attenuate the defensive cytokine response.