Cytokines in delayed-type hypersensitivity (DTH): Which lymphokines are secreted by DTH (Th1) cells to modulate macrophage function and cell migration?

Introduction / Context:
Delayed-type hypersensitivity (Type IV) reactions are orchestrated by Th1 cells that secrete cytokines to recruit, retain, and activate macrophages at the site of antigen exposure. Understanding which mediators are produced clarifies the cellular mechanisms underlying granuloma formation and tuberculin skin tests.

Given Data / Assumptions:

• DTH involves cytokines that influence macrophage behavior and leukocyte trafficking.
• Nomenclature may vary, but functions include activation, stimulation, and migration inhibition.
• Th1 profile (e.g., IFN-gamma, IL-2) underlies these effects.

Concept / Approach:
Th1 cells produce interferon-gamma, which activates macrophages (macrophage activating factor effect). Additional factors historically termed migration inhibiting factor limit macrophage egress, concentrating them at the lesion. Collectively, these cytokines enhance microbicidal activity, antigen presentation, and tissue inflammation characteristic of DTH.

Step-by-Step Solution:
Associate Th1 cytokines with macrophage activation and retention. Recognize historical terms (e.g., MIF) describing these functions. Acknowledge overlapping nomenclature but similar functional outcomes. Select the inclusive option indicating all are secreted.

Verification / Alternative check:
Experimental models show that blocking IFN-gamma reduces macrophage activation and abrogates DTH lesions, underscoring the Th1 cytokine axis.

Why Other Options Are Wrong:

• Single mediators alone do not reflect the coordinated Th1 response.
• Interleukin-4 only: More typical of Th2 responses, not DTH.

Common Pitfalls:
Assuming one cytokine is solely responsible; DTH is polycytokine-driven with synergistic effects on macrophages.

Final Answer:
All of the above.