Turner Joanne, Orme Ian M
Department of Internal Medicine, Center for Microbial Interface Biology, The Ohio State University, Columbus, OH 43210, USA.
Mech Ageing Dev. 2004 Jan;125(1):1-9. doi: 10.1016/j.mad.2003.09.002.
Old mice can express a transient early resistance to infection with M. tuberculosis that requires the presence of CD8 T cells within the lungs. Further characterization of those CD8 T cells within the aged lung established that the majority of CD8 T cells from old mice expressed the IL-15 receptor (CD122) in combination with bright expression of CD44 (CD44(hi)), and were capable of producing IFN-gamma after T cell receptor cross-linking. It has been previously described that CD8 CD44(hi) T cells proliferate in response to IFN-I, acting via IL-15, and therefore we determined whether IFN-I signaling could be a participant in the response of CD8 T cells within the lungs of old mice infected with M. tuberculosis. We demonstrate here that IFN-I signaling was required for the expansion of CD8 T cells within the aging lung in response to infection with M. tuberculosis, but that IFN-I signaling had no influence on the capacity of old mice to express early resistance to an infection with M. tuberculosis. Resident CD8 T cells were still however capable of producing IFN-gamma, which we demonstrate here to be critical in the expression of early resistance, suggesting that the expression of early resistance requires the participation, but not expansion, of the CD8 T cell pool within the aging lung.
老年小鼠可对结核分枝杆菌感染表现出短暂的早期抵抗力，这需要肺内存在CD8 T细胞。对老年肺内这些CD8 T细胞的进一步特征分析表明，老年小鼠的大多数CD8 T细胞表达白细胞介素-15受体（CD122），同时高表达CD44（CD44(hi)），并且在T细胞受体交联后能够产生干扰素-γ。先前已有报道称，CD8 CD44(hi) T细胞可通过白细胞介素-15对干扰素-I作出反应而增殖，因此我们确定干扰素-I信号传导是否可能参与感染结核分枝杆菌的老年小鼠肺内CD8 T细胞的反应。我们在此证明，干扰素-I信号传导是老年肺内CD8 T细胞响应结核分枝杆菌感染而扩增所必需的，但干扰素-I信号传导对老年小鼠对结核分枝杆菌感染表现出早期抵抗力的能力没有影响。然而，驻留的CD8 T细胞仍然能够产生干扰素-γ，我们在此证明其对早期抵抗力的表达至关重要，这表明早期抵抗力的表达需要老年肺内CD8 T细胞库的参与，但不需要其扩增。
