Причины Th2 иммунного ответа при ВИЧ-инфекции
«Protective immunity against HIV infection requires Th1 responses. The individuals with HIV infection have lower levels of glutathione (GSH) and lack of intracellular GSH leads antigen presenting cells to shift Th1 to Th2 subset in response to HIV infection. It was established that in murine macrophages, GSH depletion caused reduction of IL-12 secretion and switch from Th1 cytokine profile towards Th2 response and in human alveolar macrophages, GSH levels had a pivotal role in determining Th1 or Th2 cytokine response. Also, in human monocyte-derived DCs, the molecules able to change intracellular GSH level could augment and reduce lipopolysaccharide induced IL-27 production. Thus, expression of both IL-12 and IL-27 seem to be profoundly influenced by the redox state of APC. IL-12, produced mainly by APC, is a dominant factor in inducing the development of Th1 cells leading to secretion of IFN-γ. IL-27 is able to induce clonal proliferation of naive CD4+ T cells and synergizes with IL-12 in IFN-γ production. Additionaly, T lymphocytes that are derived from HIV infected individuals are deficient in GSH, and that this deficiency correlates with decreased levels of Th1 cytokines»
Если кратко, то причиной является дефицит глутатиона в антигенпрезентирующих клетках, которые вследствие этого в процессе активации наивных Т-хелперов продуцируют цитокины, заставляющие наивные Т-хелперы дифференцироваться как Th2.