Cell Bio Lec38 Notes p.1238-1246 T Cell Activation

T_H: macrophage activation, B stimulation to make Ab. HIV hits T_H, "...susceptible to infection by ...normally not dangerous." Dangerous = MUCH more virulent. HIV + TB= dead in 2 weeks

Recent report: HIV less virulent (analogy to myxoma in Australian rabbits).

Ag for Class II never to ER, bind to Class II (blocked and directed by invariant chain) in late endosomal compartment. Invariant chewed up. Most class II "self" bound; few foreign= enough

(only few hundred to activate class I or class II)

Dendritic, Langerhans, B cells, macrophages all "present" class II + intercellular molecules.

TCR part of CD3 complex. Signal 1 = CD3/TCR complex binding to Class II + foreign Ag

Signal 2 = signal molecule (IL-1) or, B7 (on APC)-CD28 (on T_H). Either signal alone= tolerance (analogous to learning "blocks"). Autocrine involvement of IL-2+IL-2 receptor.

T_I antigens do not activate helper T cells, so, no memory B or class switching. Low affinity Ab.

B cell endocytoses AG bound to its Ab, puts Ag onto class II molecule for TH recognition. CD40 ligand/CD40 critical for B/TH interaction. AIDS-like syndrome without this.

So, B cell needs Ag-Ab recognition + T_H stimulation to respond. Only 1 signal = block responses.

T_H1; IL-2 for T_C, macrophage stimulation. T_H2; IL-4,5 for B cells, eosinophils. Activated macrophages = "angry macrophages" in earlier literature, deal with M. tuberculosis, L. monocytogenes.

T_H memory cause TB reaction. Gamma interferon from T_H causes some cells to make class II MHC molecules and "present".