T cells in ARAP-deficient mice present defective T cell receptor signaling and reduced severity in an experimentally-induced autoimmune disease
We previously reported a novel adaptor protein, ARAP, required for T cell receptor signaling and integrin-mediated adhesion. The present study investigates further the role of ARAP in T cell biology using mice with an ARAP gene deficiency. Similar to wild-type mice, ARAP-deficient mice participate i...
Saved in:
| Main Authors: | , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Frontiers Media S.A.
2025-04-01
|
| Series: | Frontiers in Immunology |
| Subjects: | |
| Online Access: | https://www.frontiersin.org/articles/10.3389/fimmu.2025.1556616/full |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1850186486712893440 |
|---|---|
| author | Jee-Hae Kim Seung Hee Jung Chohee Park Jong Ran Lee |
| author_facet | Jee-Hae Kim Seung Hee Jung Chohee Park Jong Ran Lee |
| author_sort | Jee-Hae Kim |
| collection | DOAJ |
| description | We previously reported a novel adaptor protein, ARAP, required for T cell receptor signaling and integrin-mediated adhesion. The present study investigates further the role of ARAP in T cell biology using mice with an ARAP gene deficiency. Similar to wild-type mice, ARAP-deficient mice participate in normal breeding and immune cell development. Similar defects were observed in the T cell receptor signaling and adhesion of ARAP-deficient mice, as shown in previous studies investigating ARAP-suppressed Jurkat T cells. ARAP deficiencies analyzed in vivo presented a less severe clinical course of experimental autoimmune encephalomyelitis (EAE) following immunization of mice with the myelin oligodendrocyte glycoprotein (MOG). Serum levels of MOG-specific antibodies and IFN-γ were also reduced in ARAP-deficient EAE mice compared to wild-type EAE mice. Moreover, adoptive transfer of ARAP-deficient T cells induced less severe EAE in recombination-activating gene 1-deficient mice than wild-type T cell transfer. These results strongly suggest that ARAP positively regulates T cell function, while ARAP deficiency in T cells reduces the severity and incidence of EAE. |
| format | Article |
| id | doaj-art-77342af1a02f48c79dc71da868089ba4 |
| institution | OA Journals |
| issn | 1664-3224 |
| language | English |
| publishDate | 2025-04-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Immunology |
| spelling | doaj-art-77342af1a02f48c79dc71da868089ba42025-08-20T02:16:19ZengFrontiers Media S.A.Frontiers in Immunology1664-32242025-04-011610.3389/fimmu.2025.15566161556616T cells in ARAP-deficient mice present defective T cell receptor signaling and reduced severity in an experimentally-induced autoimmune diseaseJee-Hae KimSeung Hee JungChohee ParkJong Ran LeeWe previously reported a novel adaptor protein, ARAP, required for T cell receptor signaling and integrin-mediated adhesion. The present study investigates further the role of ARAP in T cell biology using mice with an ARAP gene deficiency. Similar to wild-type mice, ARAP-deficient mice participate in normal breeding and immune cell development. Similar defects were observed in the T cell receptor signaling and adhesion of ARAP-deficient mice, as shown in previous studies investigating ARAP-suppressed Jurkat T cells. ARAP deficiencies analyzed in vivo presented a less severe clinical course of experimental autoimmune encephalomyelitis (EAE) following immunization of mice with the myelin oligodendrocyte glycoprotein (MOG). Serum levels of MOG-specific antibodies and IFN-γ were also reduced in ARAP-deficient EAE mice compared to wild-type EAE mice. Moreover, adoptive transfer of ARAP-deficient T cells induced less severe EAE in recombination-activating gene 1-deficient mice than wild-type T cell transfer. These results strongly suggest that ARAP positively regulates T cell function, while ARAP deficiency in T cells reduces the severity and incidence of EAE.https://www.frontiersin.org/articles/10.3389/fimmu.2025.1556616/fullT cell receptor signalingadaptor proteinARAPintegrin-mediated adhesionautoimmune disease |
| spellingShingle | Jee-Hae Kim Seung Hee Jung Chohee Park Jong Ran Lee T cells in ARAP-deficient mice present defective T cell receptor signaling and reduced severity in an experimentally-induced autoimmune disease Frontiers in Immunology T cell receptor signaling adaptor protein ARAP integrin-mediated adhesion autoimmune disease |
| title | T cells in ARAP-deficient mice present defective T cell receptor signaling and reduced severity in an experimentally-induced autoimmune disease |
| title_full | T cells in ARAP-deficient mice present defective T cell receptor signaling and reduced severity in an experimentally-induced autoimmune disease |
| title_fullStr | T cells in ARAP-deficient mice present defective T cell receptor signaling and reduced severity in an experimentally-induced autoimmune disease |
| title_full_unstemmed | T cells in ARAP-deficient mice present defective T cell receptor signaling and reduced severity in an experimentally-induced autoimmune disease |
| title_short | T cells in ARAP-deficient mice present defective T cell receptor signaling and reduced severity in an experimentally-induced autoimmune disease |
| title_sort | t cells in arap deficient mice present defective t cell receptor signaling and reduced severity in an experimentally induced autoimmune disease |
| topic | T cell receptor signaling adaptor protein ARAP integrin-mediated adhesion autoimmune disease |
| url | https://www.frontiersin.org/articles/10.3389/fimmu.2025.1556616/full |
| work_keys_str_mv | AT jeehaekim tcellsinarapdeficientmicepresentdefectivetcellreceptorsignalingandreducedseverityinanexperimentallyinducedautoimmunedisease AT seungheejung tcellsinarapdeficientmicepresentdefectivetcellreceptorsignalingandreducedseverityinanexperimentallyinducedautoimmunedisease AT choheepark tcellsinarapdeficientmicepresentdefectivetcellreceptorsignalingandreducedseverityinanexperimentallyinducedautoimmunedisease AT jongranlee tcellsinarapdeficientmicepresentdefectivetcellreceptorsignalingandreducedseverityinanexperimentallyinducedautoimmunedisease |