Kumar Nathella Pavan, Moideen Kadar, Dhakshinraj Sharmila D, Banurekha Vaithilingam V, Nair Dina, Dolla Chandrakumar, Kumaran Paul, Babu Subash
National Institutes of Health-NIRT-International Centre for Excellence in Research, Chennai, India.
National Institute for Research in Tuberculosis, Chennai, India.
Immunology. 2015 Oct;146(2):243-50. doi: 10.1111/imm.12496. Epub 2015 Jul 6.
The immune system plays an important role in the pathogenesis of pulmonary tuberculosis-type 2 diabetes mellitus (PTB-DM) co-morbidity. However, the phenotypic profile of leucocyte subsets at homeostasis in individuals with active or latent tuberculosis (LTB) with coincident diabetes is not known. To characterize the influence of diabetes on leucocyte phenotypes in PTB or LTB, we examined the frequency (Fo ) of leucocyte subsets in individuals with TB with (PTB-DM) or without (PTB) diabetes; individuals with latent TB with (LTB-DM) or without (LTB) diabetes and non-TB-infected individuals with (NTB-DM) or without (NTB) diabetes. Coincident DM is characterized by significantly lower Fo of effector memory CD4(+) T cells in LTB individuals. In contrast, DM is characterized by significantly lower Fo of effector memory CD8(+) T cells and significantly higher Fo of central memory CD8(+) T cells in PTB individuals. Coincident DM resulted in significantly higher Fo of classical memory B cells in PTB and significantly higher Fo of activated memory and atypical B cells in LTB individuals. Coincident DM resulted in significantly lower Fo of classical and intermediate monocytes in PTB, LTB and NTB individuals. Finally, DM resulted in significantly lower Fo of myeloid and plasmacytoid dendritic cells in PTB, LTB and NTB individuals. Our data reveal that coincident diabetes alters the cellular subset distribution of T cells, B cells, dendritic cells and monocytes in both individuals with active TB and those with latent TB, thus potentially impacting the pathogenesis of this co-morbid condition.
免疫系统在肺结核合并2型糖尿病（PTB-DM）共病的发病机制中起重要作用。然而，合并糖尿病的活动性或潜伏性结核病（LTB）患者体内白细胞亚群在稳态时的表型特征尚不清楚。为了明确糖尿病对PTB或LTB患者白细胞表型的影响，我们检测了合并（PTB-DM）或未合并（PTB）糖尿病的结核病患者、合并（LTB-DM）或未合并（LTB）糖尿病的潜伏性结核病患者以及合并（NTB-DM）或未合并（NTB）糖尿病的非结核感染个体的白细胞亚群频率（Fo）。合并糖尿病的特征是LTB个体中效应记忆CD4(+) T细胞的Fo显著降低。相比之下，糖尿病的特征是PTB个体中效应记忆CD8(+) T细胞的Fo显著降低，而中枢记忆CD8(+) T细胞的Fo显著升高。合并糖尿病导致PTB患者中经典记忆B细胞的Fo显著升高，LTB个体中活化记忆B细胞和非典型B细胞的Fo显著升高。合并糖尿病导致PTB、LTB和NTB个体中经典单核细胞和中间单核细胞的Fo显著降低。最后，糖尿病导致PTB、LTB和NTB个体中髓样树突状细胞和浆细胞样树突状细胞的Fo显著降低。我们的数据表明，合并糖尿病会改变活动性结核病患者和潜伏性结核病患者体内T细胞、B细胞、树突状细胞和单核细胞的细胞亚群分布，从而可能影响这种共病情况的发病机制。
