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Targeting the balance of T helper cell responses by curcumin in inflammatory and autoimmune states

Rahimi, Kaveh; Ahmadi, Abbas; Hassanzadeh, Kambiz; Soleimani, Zahra; Sathyapalan, Thozhukat; Mohammadi, Asadollah; Sahebkar, Amirhossein


Kaveh Rahimi

Abbas Ahmadi

Kambiz Hassanzadeh

Zahra Soleimani

Thozhukat Sathyapalan

Asadollah Mohammadi

Amirhossein Sahebkar


CD4+ T helper (Th) cells are a crucial player in host defense but under certain conditions can contribute to the pathogenesis of inflammatory and autoimmune diseases. Beside the Th1/Th2 subset, several additional Th subsets have been identified, each with a distinctive transcription factor, functional properties, signature cytokine profile, and possible role in the pathophysiology of diseases. These newer Th subsets include Th17, regulatory Th cells (Tregs), and more recently, Th9, Th22, and follicular T helper cells. Interestingly, imbalance of Th subsets contributes to the immunopathology of several disease states. Therefore, targeting the imbalance of Th subsets and their signature cytokine profiles by a safe, effective and inexpensive nutraceutical agent such as curcumin could be helpful to treat autoimmune and inflammatory diseases. In this study different Th subsets and how the imbalance of these subsets could promote pathology of several diseases has been reviewed. Furthermore, the role of curcumin in this process will be discussed and the impact of targeting Th subsets by curcumin.

Journal Article Type Article
Publication Date 2019-05
Journal Autoimmunity Reviews
Print ISSN 1568-9972
Publisher Elsevier
Peer Reviewed Peer Reviewed
Institution Citation Rahimi, K., Ahmadi, A., Hassanzadeh, K., Soleimani, Z., Sathyapalan, T., Mohammadi, A., & Sahebkar, A. (2019). Targeting the balance of T helper cell responses by curcumin in inflammatory and autoimmune states. Autoimmunity Reviews,
Keywords Immunology; Immunology and Allergy
Publisher URL
Additional Information ©2019, Elsevier. This manuscript version is made available under the CC-BY-NC-ND 4.0 license