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Bee venom stirs up buzz in antigen presentation.

Van Kaer L - J. Exp. Med. (2015)

View Article: PubMed Central - HTML - PubMed

Affiliation: Vanderbilt University School of Medicine luc.van.kaer@vanderbilt.edu.

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In this issue, Bourgeois et al. establish the concept that enzymes in bee venom can cleave host skin-derived phospholipids into lipid neoantigens that activate CD1a-restricted T cells to promote a local inflammatory response... In searching for potential contributions of CD1a-reactive T cells to inflammatory responses in the skin, Bourgeois et al. investigated human T cell responses to the venoms of bees and wasps... They found that such venoms induce a CD1a-mediated response in both individual T cell clones and primary human T cells... These intriguing findings support a model of T cell activation involving insect-mediated PLA2 introduction into the skin, inducing the release of fatty acid neoantigens from common skin phospholipids, subsequently sampled by Langerhans cells, loaded onto CD1a molecules, and presented to T cells... In this manner, CD1a-reactive T cells may contribute to the local inflammatory response to venoms... The findings also provide a potential molecular explanation for the generation of autoantigens in normal skin, which expresses secreted phospholipases... It has been proposed that such natural lipids are present at the surface of the skin and are thus inaccessible to CD1a-restricted T cells in the dermis... However, a breach in the skin barrier might make these natural oils available to Langerhans cells in the epidermis, resulting in their presentation to CD1a-reactive T cells and the subsequent induction of antimicrobial and inflammatory responses... Moreover, infections and inflammatory processes can modulate the expression patterns of phospholipases in the skin, which may represent a mechanism to control inflammation via CD1a-reactive T cells... Finally, certain skin pathogens secrete PLA2 enzymes, raising the possibility that such infections can induce CD1a-mediated T cell responses that contribute to host immunity and disease pathogenesis... These proposed scenarios, together with their potential therapeutic applications, will provide rich and fertile avenues for future investigation.

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Phospholipase A2 (PLA2) in bee venom is introduced into human skin and cleaves ubiquitous phospholipids into free fatty acids and lysophospholipids that function as neoantigens. These fatty acid neoantigens are now available for sampling by epidermal Langerhans cells, which load them onto CD1a proteins and present them at their surface to skin-resident CD1a-reactive T cells. These T cells produce cytokines such as IL-22 that contribute to the inflammatory response.
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fig2: Phospholipase A2 (PLA2) in bee venom is introduced into human skin and cleaves ubiquitous phospholipids into free fatty acids and lysophospholipids that function as neoantigens. These fatty acid neoantigens are now available for sampling by epidermal Langerhans cells, which load them onto CD1a proteins and present them at their surface to skin-resident CD1a-reactive T cells. These T cells produce cytokines such as IL-22 that contribute to the inflammatory response.


Bee venom stirs up buzz in antigen presentation.

Van Kaer L - J. Exp. Med. (2015)

Phospholipase A2 (PLA2) in bee venom is introduced into human skin and cleaves ubiquitous phospholipids into free fatty acids and lysophospholipids that function as neoantigens. These fatty acid neoantigens are now available for sampling by epidermal Langerhans cells, which load them onto CD1a proteins and present them at their surface to skin-resident CD1a-reactive T cells. These T cells produce cytokines such as IL-22 that contribute to the inflammatory response.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4322043&req=5

fig2: Phospholipase A2 (PLA2) in bee venom is introduced into human skin and cleaves ubiquitous phospholipids into free fatty acids and lysophospholipids that function as neoantigens. These fatty acid neoantigens are now available for sampling by epidermal Langerhans cells, which load them onto CD1a proteins and present them at their surface to skin-resident CD1a-reactive T cells. These T cells produce cytokines such as IL-22 that contribute to the inflammatory response.

View Article: PubMed Central - HTML - PubMed

Affiliation: Vanderbilt University School of Medicine luc.van.kaer@vanderbilt.edu.

AUTOMATICALLY GENERATED EXCERPT
Please rate it.

In this issue, Bourgeois et al. establish the concept that enzymes in bee venom can cleave host skin-derived phospholipids into lipid neoantigens that activate CD1a-restricted T cells to promote a local inflammatory response... In searching for potential contributions of CD1a-reactive T cells to inflammatory responses in the skin, Bourgeois et al. investigated human T cell responses to the venoms of bees and wasps... They found that such venoms induce a CD1a-mediated response in both individual T cell clones and primary human T cells... These intriguing findings support a model of T cell activation involving insect-mediated PLA2 introduction into the skin, inducing the release of fatty acid neoantigens from common skin phospholipids, subsequently sampled by Langerhans cells, loaded onto CD1a molecules, and presented to T cells... In this manner, CD1a-reactive T cells may contribute to the local inflammatory response to venoms... The findings also provide a potential molecular explanation for the generation of autoantigens in normal skin, which expresses secreted phospholipases... It has been proposed that such natural lipids are present at the surface of the skin and are thus inaccessible to CD1a-restricted T cells in the dermis... However, a breach in the skin barrier might make these natural oils available to Langerhans cells in the epidermis, resulting in their presentation to CD1a-reactive T cells and the subsequent induction of antimicrobial and inflammatory responses... Moreover, infections and inflammatory processes can modulate the expression patterns of phospholipases in the skin, which may represent a mechanism to control inflammation via CD1a-reactive T cells... Finally, certain skin pathogens secrete PLA2 enzymes, raising the possibility that such infections can induce CD1a-mediated T cell responses that contribute to host immunity and disease pathogenesis... These proposed scenarios, together with their potential therapeutic applications, will provide rich and fertile avenues for future investigation.

Show MeSH
Related in: MedlinePlus