Human Immune Response and Tolerance Compensating for the Adverse Impacts of Climate Change on Human Respiratory Health and Autoimmunity
Journal Title: Journal of Clinical Immunology & Microbiology - Year 2025, Vol 6, Issue 1
Abstract
Climate change is a burning issue which we cannot overlook. Environmental stressors, antigens, pollens, particulate matter, ground-level ozone O3, heat waves, wildfires, floods, drought, altered rainfall patterns, hurricanes, thunderstorms, windstorms, air pollution and increased pathogens are some climate change outcomes. Now, the problem is how the human immune responds to continuous exposure to such stressors and Pathogen-Associated Molecular Patterns (PAMPs). Our human body has evolved in such a way that innate and acquired both cell-mediated and humoral immunity adaptive mechanisms to detect and eliminate such foreign particles. The most common response to pollen exposure is manifested as allergies, in which the body responds to allergens like pollens by activating mast cells to secrete histamine. Exposure of the body, skin and lungs to allergens causes an impaired epithelial barrier, which permits entry of allergens, pollutants, antigens and bacterial endotoxins, causing the release of cytokines IL-25, IL-33 and TSLP. Th2 cytokines IL-4, IL-5, IL-9 and IL-13, in turn, activate B-cells to produce antibodies IgE, including other isotypes (IgG, IgA and IgG4) and T cells as well activate mast cells. Mast cells express a variety of receptors, including high-affinity FcεRI receptors, to recognize a wide range of foreign molecules. Two important events are possible in response to IgE-FcεRI stimulation: 1). release of proteoglycans, proteases and neuropeptides from the granules due to intracellular Ca2⁺ levels mediated by phosphorylation of Phospholipase C Gamma 1 (PLC-γ1) and 2). activation of nuclear factor kappa B (NF-κB) mediates the secretion of de novo synthesized lipid mediators and cytokines. It enhances the expression of numerous inflammation-related genes mediated by the major transcription factor. The function of all these factors is to act together in order to control inflammation. Difficult respiratory diseases, chronic respiratory allergic diseases such as asthma, sensitization to aero and food allergens and the development of eczema and hay fever, allergic rhinoconjunctivitis and sinusitis characterized by repeated sneezing are related to inhalation of environmental stimulants pollutants, dust, smoke and toxins particles with an aerodynamic diameter of about 0.003 to 5 µm that can penetrate deep inside the alveoli of the lungs, affecting gaseous exchange and thereby reducing O2 availability to body tissues. The gut microbiome can also be altered due to multiple climate change-related factors changing the way antigen specific suppression of immune response involving B and T-lymphocytes. Prolonged heat wave exposure is a major problem that can elicit oxidative stress by producing Reactive Oxygen Species (ROS), causing DNA damage and upregulation of Heat Shock Protein (HSP) genes expressing molecular chaperons. HSP proteins exacerbate acute and chronic inflammation. Moreover, due to climate change and environmental alterations many parts of the world are now facing increased autoimmune and autoimmune diseases. Autoimmunity is a condition in which self-cells start attacking their own cells, if pathogens are also helping in the process called autoimmune diseases. Environmental factors such as tissue damage and infection can trigger and interact with genetic factors to induce autoimmunity. The human body establishes its own adaptive mechanisms after prolonged contact with such stressors and may become immune tolerant by deleting reactive lymphocytes and generating regulatory T (Treg) cells. The development and maintenance of immune tolerance is critical because it can cause many diseases. Our knowledge of understanding is limited as there may be multiple synergistic interactions and various factors can simultaneously act together to trigger such immune responses.
Authors and Affiliations
Salam Himika Devi1*
Keywords
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- EP ID EP761821
- DOI http://dx.doi.org/10.46889/JCIM.2025.6105
- Views 28
- Downloads 0
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