What would result from an IL-12 receptor deficiency?

• A. Decreased Th1 response and IFN-γ
• B. Increased Th1 response
• C. Decreased Th17 response
• D. Hyper IgE syndrome

Answer: (A)

IL-12 signaling directs naive T cells to become Th1 cells and stimulates NK and T cells to produce IFN-γ through the STAT4 pathway. If the IL-12 receptor is defective, this signaling is blunted, so Th1 differentiation is impaired and IFN-γ production falls. That reduces the ability to mount cell-mediated responses against intracellular pathogens like mycobacteria. The other options don’t fit because increasing Th1 would require intact signaling, and while IL-12 receptor deficiency can affect other pathways (like IL-23 signaling that shares the receptor subunit and can influence Th17 cells), the hallmark outcome is a diminished Th1 response with reduced IFN-γ. Hyper IgE syndrome comes from STAT3-related mechanisms, not IL-12 receptor defects.