Putative pathophysiologic roles of CA-induced alterations of Th1/Th2 balance in certain infections, infectious complications after major injury, autoimmune/inflammatory, allergic or neoplastic diseases (modified from Elenkov and Chrousos, 1999)
| Condition | Host Response | Pathogenic Response | Role of CAs and Stress |
|---|---|---|---|
| Infections | Th1 protects | Suppressed cellular immunity, deficit of IL-12 and IFN-γ, Th2 shift with progression of infection | Stress-induced increase of CAs levels and subsequent Th2 shift may contribute to increased susceptibility to or progression of these infections |
| Mycobacterium tuberculosis | |||
| Helicobacterium pylori | |||
| HIV | |||
| Common cold viruses | |||
| Major injury | Th2 protects? | Suppressed cellular immunity and IL-12, and IFN-γ production, overproduction of IL-10, Th2 shift | Increased levels of CAs may contribute to suppression of cellular immunity resulting in infectious complications |
| Autoimmunity | Excessive Th1 response | Th1 shift, overproduction of IL-12, TNF-α, IFN-γ; deficit of IL-10 | A hypoactive SNS may facilitate/sustain the Th1 shift and flares of these autoimmune diseases5-a |
| Rheumatoid arthritis | |||
| Multiple sclerosis | |||
| Autoimmune thyroid disease | |||
| Type 1 diabetes mellitus | |||
| Tumors | Th1 protects | Suppressed cellular immunity, deficit of IL-12, TNF-α, overproduction of IL-10 and TGF-β | Hyperactive SNS and CA-induced Th2 shift may contribute to increased susceptibility to or progression of certain tumors |
↵5-a The role of SNS in autoimmunity is more complex; see text for details.