Climate extremes are increasingly shaping both environmental and human health outcomes. Global warming has led to a rise in the frequency, duration, and intensity of extreme temperature events, with heatwaves emerging as one of the most hazardous weather-related threats. Beyond their well-recognized cardiovascular and respiratory effects, heat extremes are now understood to influence immune function. Growing evidence indicates that heat extremes along with air pollution, wildfires, humidity shifts, and ecosystem disruption can impair epithelial barrier integrity and disturb immune regulation. These stressors may promote chronic inflammation, alter adaptive immune responses, and compromise host defense mechanisms. Experimental and epidemiological data suggest that heat stress can reduce effective B-cell responses, modify antigen presentation, and increase inflammatory signaling, while combined exposures to heat and pollutants may further increase susceptibility to infectious, allergic, and autoimmune diseases. Although the physical drivers of climate change are well established, the biological pathways linking environmental stressors to immune dysregulation remain incompletely defined. This review synthesizes current evidence on the mechanisms by which extreme heat events influence immune tolerance and disease risk. We discuss implications for allergy, autoimmunity, and infectious diseases, highlight vulnerable populations, and outline key research priorities needed to inform clinical and public health adaptation.
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