Commentary: adaptive immunity in the absence of innate immune responses? The un-Tolled truth of the silent invaders.
The development and expression of effective adaptive immunity is currently thought to hinge entirely upon inductor and effector mechanisms furnished by cells of the innate immune system. An obligate intracellular bacterium, the causative agent of human granulocytic anaplasmosis, apparently defies this dogma: in a mouse model of infection, Anaplasma phagocytophilum is controlled by specific lymphocyte immunity even in the absence of Toll-like receptor (TLR)2, TLR4, the TLR-adaptor protein MyD88, inducible nitric oxide synthase or the gp91 component of the NADPH oxidase complex. A. phagocytophilum infection biology raises some interesting questions about the development of resistance to innate defense strategies by vector-borne pathogens, and challenges our current bias concerning the relative importance and the mode of interaction of the innate and adaptive arms of infection control in vertebrates.
Ehlers
Stefan
S
Molecular Infection Biology, Research Center Borstel, Leibniz Center for Medicine and Biosciences, Borstel, Germany. sehlers@fz-borstel.de
D041081:Anaplasma phagocytophilum / Q000276:immunology*; D000818:Animals; D005075:Biological Evolution; D006801:Humans; D007109:Immunity / Q000276:immunology*; D007113:Immunity, Innate / Q000276:immunology; D008562:Membrane Glycoproteins / Q000172:deficiency* / Q000378:metabolism; D011956:Receptors, Cell Surface / Q000172:deficiency* / Q000378:metabolism; D051195:Toll-Like Receptor 2; D051197:Toll-Like Receptor 4; D051193:Toll-Like Receptors
D008562:Membrane Glycoproteins; D011956:Receptors, Cell Surface; C495342:TLR2 protein, human; C495345:TLR4 protein, human; D051195:Toll-Like Receptor 2; D051197:Toll-Like Receptor 4; D051193:Toll-Like Receptors