Abstract
AMONG the numerous T-cell defects identified in patients with the acquired immunodeficiency syndrome (AIDS),1 the failure to generate gamma interferon2 seems likely for several reasons to be relevant to the immunopathogenesis of AIDS-related opportunistic infections. For example, gamma interferon is probably the key T-cell-derived lymphokine that induces macrophages and other potential host defense cells to exert enhanced antimicrobial activity against both intracellular and extracellular pathogens.3 4 5 6 7 8 9 10 In addition, gamma interferon also appears to have a pivotal regulatory role in a variety of other cellular immune reactions,11 including those involved in antigen-stimulated T-cell activation.12 13 14 15 Given this background and the earlier demonstration that.
| Original language | English |
|---|---|
| Pages (from-to) | 1504-1510 |
| Number of pages | 7 |
| Journal | New England Journal of Medicine |
| Volume | 313 |
| Issue number | 24 |
| DOIs | |
| State | Published - 12 Dec 1985 |
| Externally published | Yes |