Human immunodeficiency virus-tuberculosis (HIV-TB) co-infection poses a challenge to the immunologists in developing new diagnostic and therapeutic tools. Mechanisms behind the breakdown of the immune defense of the co-infected individual are poorly known. Numerous studies in HIV alone have revealed the role of PD1, TAP, and IL-10, but not in co-infection. The interaction of the 2 distinct bugs, which is resulting in domination over the host immune system, is still a lacuna. Hence, we aimed to portray functions of IL-10, TAP, and PD1 molecules in HIV-TB co-infection. Co-culture cells challenged with γ-irradiated M.Tb under various conditions resulted in high interleukin (IL)-10 secretion and high percentage of PD1 expression on CD8 T cells, which might be due to defective antigen presentation of TAP on dendritic cells and macrophages. Herein our observations provide an insight into the escape mechanisms by M.Tb in HIV-infected individuals from the host immune responses leading to TB co-infection.

中文翻译：

---

缺陷抗原呈递导致HIV-TB合并感染中PD1和IL-10的上调。

人类免疫缺陷病毒-结核（HIV-TB）合并感染在开发新的诊断和治疗工具方面给免疫学家带来了挑战。共同感染的个体的免疫防御能力崩溃的机制鲜为人知。仅在HIV方面的大量研究就已经揭示了PD1，TAP和IL-10的作用，但在共感染中却没有。导致宿主免疫系统支配的2个不同的bug的相互作用仍然是一个空白。因此，我们旨在描绘IL-10，TAP和PD1分子在HIV-TB合并感染中的功能。共培养细胞经γ射线照射的M.Tb攻击在各种条件下会导致CD8 T细胞上高白介素（IL）-10分泌和PD1表达的高百分比，这可能是由于TAP在树突状细胞和巨噬细胞上的抗原呈递不足所致。在本文中，我们的观察提供了从M.Tb在HIV感染个体中逃逸导致宿主共同免疫的宿主免疫反应的逃逸机制的见解。