Journal
JOURNAL OF INFECTIOUS DISEASES
Volume 198, Issue 10, Pages 1514-1519Publisher
OXFORD UNIV PRESS INC
DOI: 10.1086/592448
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Funding
- Howard Hughes Medical Institute Funding Source: Medline
- NCRR NIH HHS [R01 RR013601-05, R01 RR013601-038515, R01 RR013601, R01 RR013601-02, R01 RR013601-10, RR13601] Funding Source: Medline
- NHLBI NIH HHS [HL64560, R01 HL064560-05, R01 HL064560, R01 HL064560-02, R01 HL064560-07, R01 HL064560-06] Funding Source: Medline
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The immune mechanisms by which early host-mycobacterium interaction leads to the development of severe tuberculosis (TB) remain poorly characterized in humans. Here, we demonstrate that severe TB in juvenile rhesus monkeys down-regulated many genes in the blood but up-regulated selected genes constituting gene networks of Th17 and Th1 responses, T cell activation and migration, and inflammation and chemoattractants in the pulmonary and lymphoid compartments. Overexpression (450-2740-fold) of 13 genes encoding inflammatory cytokines and receptors (IL-22, CCL27, MIP-1 alpha, IP-10, CCR4, CCR5, and CXCR3), immune dysfunctional receptors and ligands (PD1 and PDL2), and immune activation elements (IL-3, IFN-beta, TIM1, and TLR2) was seen in tissues, with low antigen-specific cellular responses. Thus, severe TB in macaques features unbalanced up-regulation of immune-gene networks without proportional increases in antigen-specific cellular responses.
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