Browsing by Author "Pradeep Kumar Das"

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Antigens activated SOCS3+CD200R+CD4+ T cells are critical to Leishmania pathogenesis and a distinctive target for vaccine development
(Elsevier Ltd, 2025) Abhishek Kumar Singh; Baishakhi Mahapatra; Ankita Srivastava; Samer Singh; Pradeep Kumar Das; Rakesh Kumar Singh
The expression of suppression of cytokine signalling protein (SOCS3) has been posited as a critical determinant of T cells differentiation and maturation during visceral leishmaniasis (VL), however, the antigen-activated CD4+ T cell phenotypes expressing this protein have not been explored much. Since, the inherent nature of SOCS3 protein directs the polarization of CD4+ T cells towards anti-inflammatory Th2 axis, the identification of SOCS3 expressing T-cell phenotypes will provide a better understanding on Leishmania immunobiology. Our previous findings have delineated a distinct Leishmania antigens activated CD4+ T cells phenotype expressing CD200R receptor that acts as prime anti-inflammatory disease promoting subset. Here, in this study we observed that the SOCS3+ antigen activated CD200R+CD4+ T cells phenotype is succinctly involved in cytokines regulation during Leishmania infection. We further observed that CD200R+CD4+ T cells expressing higher levels of SOCS3 protein have the potential to polarize these cells to produce more IL-10, and less IL-12 & IFN-γ as compared to CD200R−CD4+T cells on exposure to whole killed Leishmania vaccine in a mice model of VL. Furthermore, the observed decline in splenic SOCS3 expression along with inflammatory factors like prostaglandin E2, upon abrogation of CD200R signalling in Leishmania infected animals suggest a coordinated role of CD200R and SOCS3 protein in VL pathogenesis. These findings prompted us to study the potential of CD200R and SOCS3 in the vaccine-induced immunity. Immunization with an in-house whole killed Leishmania vaccine adjuvanted with anti-CD200 antibodies not only reduced splenic SOCS3 expression but also enhanced CD4+ T cells' effector functions and their memory conversion. The down-regulation of splenic SOCS3 was also found correlated with reduced granuloma and parasitic load in SOCS3-low mice groups. Hence, the identified SOCS3+CD200R+CD4+ T cells subset reveals a potential disease-promoting phenotype that can be targeted to enhance the immunogenicity of Leishmania antigens. © 2025
Corrigendum to “Antigens activated SOCS3+CD200R+CD4+ T cells are critical to Leishmania pathogenesis and a distinctive target for vaccine development” [Vaccine 62 (2025) 127501] (Vaccine (2025) 62, (S0264410X25007984), (10.1016/j.vaccine.2025.127501))
(Elsevier Ltd, 2025) Abhishek Kumar Singh; Baishakhi Mahapatra; Ankita Srivastava; Samer Singh; Pradeep Kumar Das; Rakesh Kumar Singh
The authors regret the error in the acknowledgements in the published article (DOI: https://doi.org/10.1016/j.vaccine.2025.127501). The original text: This work is an output of a project funded to RKS by the Indian Council of Medical Research, New Delhi (No. VIR/12/2022/ECD-1). AS and BM are thankful to UP-CST, Lucknow, and DBT, New Delhi, respectively for their research fellowships. RKS also acknowledges the support received under the Institute of Eminence (IoE 6031), Central Government of India, and Uttar Pradesh council of science and technology (UP-CST/D-2245) for financial assistance. The corrected version: This work is an output of a project funded to RKS by the Indian Council of Medical Research, New Delhi (No. VIR/12/2022/ECD-1). AS and BM are thankful to UP-CST, Lucknow, and DBT, New Delhi, respectively for their research fellowships. RKS also acknowledges the support received under the Institute of Eminence (IoE 6031), Central Government of India, and Uttar Pradesh council of science and technology (UP-CST/D-2245) for financial assistance. PD, the recipient of ICMR-Emeritus Scientist, acknowledges the support of ICMR, New Delhi. This amendment ensures proper acknowledgement of contributions. We sincerely apologize for any inconvenience caused and thank the editors for their understanding. © 2025 Elsevier Ltd