Figure 1:

Schematic representation of the potential direct and indirect pathways through which UVBR can influence immune function in amphibian early life stages. UVBR can directly kill and damage cells in the outer skin layers, disrupting the physical integrity of the skin, compromising the function of cutaneous dendritic cells (D) and leucocytes (L), and triggering exposed keratinocytes (K) to release a cascade of immunosuppressive molecules that inhibit innate and adaptive immune functions of the systemic immune system. UVBR can disrupt the innate immune function of the cutaneous ‘secretome’ (mucus, antimicrobial peptides, complement, lysozyme, etc.) and influence the composition of the host microbiome. Indirectly, UVBR may influence immune function via its impact on interrelated physiological systems. For example, UVBR can affect immune function by disrupting energy production and/or distribution pathways, by influencing neuroendocrine signalling pathways controlling immune system maturation or inducing a physiological stress response (involving glucocorticoids). UVRB-associated damage to DNA and other biomolecules may also have a lasting impact on immune function by influencing gene expression patterns in subsequent life stages. Image: Cameron Baker©.