Decreased percentage of CD4+ lymphocytes expressing chemokine receptors in bipolar disorder

Izabela G. Barbosa, Natalia P. Rocha, Erica L. Vieira, Mehmet A. Camkurt, Rodrigo B. Huguet, Fabio T.L. Guimarães, Gustavo E. De Brito-Melo, Vanessa A. Mendonça, Moises E. Bauer, Antonio L. Teixeira

Research output: Contribution to journalArticlepeer-review

7 Scopus citations


Objective: Although accumulating evidence supports the hypothesis that immune/inflammatory mechanisms are associated with the pathophysiology of bipolar disorder (BD), data about the profile of chemokines (chemotactic cytokines) and chemokine receptors are still scarce. The current study was designed to evaluate the expression of chemokine receptors on lymphocytes of patients with BD in comparison with controls.Methods: Thirty-three patients with type I BD (N = 21 in euthymia; N = 6 in mania/hypomania; N = 6 in depression) and 22 age- and sex-matched controls were subjected to clinical evaluation and peripheral blood draw. The expression of chemokine receptors CCR3, CCR5, CXCR4, and CXCR3 on CD4+ and CD8+ lymphocytes was assessed by flow cytometry.Results: Patients with BD had decreased percentage of CD4+CXCR3+ (p = 0.024), CD4+CCR3+ (p = 0.042), and CD4+CCR5+ (0.013) lymphocytes in comparison with controls. The percentage of both CD4+ and CD8+ lymphocytes expressing the chemokine receptor CXCR4 was similar in patients with BD and controls. Likewise, the percentages of CD8+CXCR3+, CD8+CCR3+, and CD8+CCR5+ lymphocytes were similar in patients with BD and controls.Conclusion: Our findings reinforce the hypothesis that immune pathways, especially involving CD4+ lymphocytes, are involved in the physiopathology of BD.

Original languageEnglish (US)
Pages (from-to)246-251
Number of pages6
JournalActa Neuropsychiatrica
Issue number5
StatePublished - Oct 1 2019
Externally publishedYes


  • bipolar disorder
  • chemokine receptors
  • lymphocytes
  • psychoneuroimmunology

ASJC Scopus subject areas

  • Psychiatry and Mental health
  • Biological Psychiatry


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