The response of CD1d-restricted invariant NKT cells to microbial pathogens and their products
Invariant natural killer T (iNKT) cells become activated during a wide variety of infections. This includes organisms lacking cognate CD1d-binding glycolipid antigens recognized by the semi-invariant T cell receptor of iNKT cells. Additional studies have shown that iNKT cells also become activated i...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2015-05-01
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| Series: | Frontiers in Immunology |
| Subjects: | |
| Online Access: | http://journal.frontiersin.org/Journal/10.3389/fimmu.2015.00226/full |
| _version_ | 1819111353169739776 |
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| author | Luc eVan Kaer Vrajesh eParekh Lan eWu |
| author_facet | Luc eVan Kaer Vrajesh eParekh Lan eWu |
| author_sort | Luc eVan Kaer |
| collection | DOAJ |
| description | Invariant natural killer T (iNKT) cells become activated during a wide variety of infections. This includes organisms lacking cognate CD1d-binding glycolipid antigens recognized by the semi-invariant T cell receptor of iNKT cells. Additional studies have shown that iNKT cells also become activated in vivo in response to microbial products such as bacterial lipopolysaccharide, a potent inducer of cytokine production in antigen-presenting cells (APCs). Other studies have shown that iNKT cells are highly responsive to stimulation by cytokines such as interleukin-12. These findings have led to the concept that microbial pathogens can activate iNKT cells either directly via glycolipids, or indirectly by inducing cytokine production in APCs. iNKT cells activated in this manner produce multiple cytokines that can influence the outcome of infection, usually in favor of the host, although potent iNKT cell activation may contribute to an uncontrolled cytokine storm and sepsis. One aspect of the response of iNKT cells to microbial pathogens is that it is short-lived and followed by an extended time period of unresponsiveness to reactivation. This refractory period may represent a means to avoid chronic activation and cytokine production by iNKT cells, thus protecting the host against some of the negative effects of iNKT cell activation, but potentially putting the host at risk for secondary infections. These effects of microbial pathogens and their products on iNKT cells are not only important for understanding the role of these cells in immune responses against infections but also for the development of iNKT cell-based therapies. |
| first_indexed | 2024-12-22T03:56:16Z |
| format | Article |
| id | doaj.art-30be11bf2b264780afcddb3cd8bcfefa |
| institution | Directory Open Access Journal |
| issn | 1664-3224 |
| language | English |
| last_indexed | 2024-12-22T03:56:16Z |
| publishDate | 2015-05-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Immunology |
| spelling | doaj.art-30be11bf2b264780afcddb3cd8bcfefa2022-12-21T18:39:51ZengFrontiers Media S.A.Frontiers in Immunology1664-32242015-05-01610.3389/fimmu.2015.00226146418The response of CD1d-restricted invariant NKT cells to microbial pathogens and their productsLuc eVan Kaer0Vrajesh eParekh1Lan eWu2Vanderbilt UniversityVanderbilt UniversityVanderbilt UniversityInvariant natural killer T (iNKT) cells become activated during a wide variety of infections. This includes organisms lacking cognate CD1d-binding glycolipid antigens recognized by the semi-invariant T cell receptor of iNKT cells. Additional studies have shown that iNKT cells also become activated in vivo in response to microbial products such as bacterial lipopolysaccharide, a potent inducer of cytokine production in antigen-presenting cells (APCs). Other studies have shown that iNKT cells are highly responsive to stimulation by cytokines such as interleukin-12. These findings have led to the concept that microbial pathogens can activate iNKT cells either directly via glycolipids, or indirectly by inducing cytokine production in APCs. iNKT cells activated in this manner produce multiple cytokines that can influence the outcome of infection, usually in favor of the host, although potent iNKT cell activation may contribute to an uncontrolled cytokine storm and sepsis. One aspect of the response of iNKT cells to microbial pathogens is that it is short-lived and followed by an extended time period of unresponsiveness to reactivation. This refractory period may represent a means to avoid chronic activation and cytokine production by iNKT cells, thus protecting the host against some of the negative effects of iNKT cell activation, but potentially putting the host at risk for secondary infections. These effects of microbial pathogens and their products on iNKT cells are not only important for understanding the role of these cells in immune responses against infections but also for the development of iNKT cell-based therapies.http://journal.frontiersin.org/Journal/10.3389/fimmu.2015.00226/fullImmunotherapymicrobial pathogensCD1dmicrobial productsinvariant natural killer T cellsGlycolipid antigens |
| spellingShingle | Luc eVan Kaer Vrajesh eParekh Lan eWu The response of CD1d-restricted invariant NKT cells to microbial pathogens and their products Frontiers in Immunology Immunotherapy microbial pathogens CD1d microbial products invariant natural killer T cells Glycolipid antigens |
| title | The response of CD1d-restricted invariant NKT cells to microbial pathogens and their products |
| title_full | The response of CD1d-restricted invariant NKT cells to microbial pathogens and their products |
| title_fullStr | The response of CD1d-restricted invariant NKT cells to microbial pathogens and their products |
| title_full_unstemmed | The response of CD1d-restricted invariant NKT cells to microbial pathogens and their products |
| title_short | The response of CD1d-restricted invariant NKT cells to microbial pathogens and their products |
| title_sort | response of cd1d restricted invariant nkt cells to microbial pathogens and their products |
| topic | Immunotherapy microbial pathogens CD1d microbial products invariant natural killer T cells Glycolipid antigens |
| url | http://journal.frontiersin.org/Journal/10.3389/fimmu.2015.00226/full |
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