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Clonal expansion of CD8+ T cells in Kawasaki disease
I H Choi1, Y J Chwae, W S Shim
1Department of Microbiology, Yonsei University College of Medicine, Seodaemoon-ku, Seoul, Korea. inhong@yumc.yonsei.ac.kr
Insights
Kawasaki disease (KD) pathogenesis may involve conventional antigens, not superantigens. Studies found T cell clonal expansions during acute KD, which resolved over time, suggesting a non-superantigenic immune response.
Area of Science:
- Pediatric Cardiology
- Immunology
- Infectious Disease Etiology
Background:
- Kawasaki disease (KD) is a leading cause of acquired heart disease in children.
- The exact infectious etiology of KD remains unclear.
- KD involves immune activation, including T cells, monocytes, macrophages, and elevated cytokines.
Purpose of the Study:
- To investigate the role of superantigens in Kawasaki disease pathogenesis.
- To analyze T cell clonal expansion during different phases of KD.
Main Methods:
- Examined complementarity-determining region 3 (CDR3) size profiles of T cells expressing various TCRBV chains (TCRBV1, 2, 4, 5, 8, 14, 16, 17, 18, 20).
- Assessed T cell populations during acute KD, subacute KD, and long-term follow-up.
- Focused on CD8+ T cells.
Main Results:
- Observed significant T cell clonal expansions, primarily in CD8+ T cells, during the acute phase of KD.
- These expansions were transient and disappeared during the long-term follow-up period.
- The pattern of T cell expansion did not strongly support a superantigen-driven mechanism.
Conclusions:
- The findings suggest that conventional antigens, rather than superantigens, are likely involved in the pathogenesis of acute Kawasaki disease.
- Further research is needed to elucidate the specific antigens triggering the immune response in KD.
Abstract:
Kawasaki disease (KD) is the major cause of acquired heart disease in children. KD is suspected of being an infectious disease, but the etiology has not yet been clarified. Immunologically, the disease is associated with the activation of T cells, monocytes, and macrophages resulting in highly elevated levels of several cytokines. Recently, expansions of T cells expressing TCRBV2 and TCRBV8 chains have been reported, and this suggests the involvement of a superantigen in the pathogenesis of KD. To address the role of a superantigen in KD, we investigated clonal expansion of T cells by estimating the complementarity-determining region 3 size profile among T cells expressing TCRBV1, TCRBV2, TCRBV4, TCRBV5, TCRBV8, TCRBV14, TCRBV16, TCRBV17, TCRBV18, and TCRBV20 chains during acute KD, during subacute KD, and during the long term follow-up period. During the acute phase of KD, several clonal expansions were found mainly in the CD8+ T cells that disappeared during the long term follow-up period. Our data suggest that the conventional Ags rather than a superantigen were involved in the pathogenesis of acute KD.