Case report: Kikuchi-Fujimoto disease: unveiling a case of recurrent fever and enlarged cervical lymph nodes in a young female patient with a literature review of the immune mechanism

Front Immunol. 2024 Jan 19:14:1279592. doi: 10.3389/fimmu.2023.1279592. eCollection 2023.

Abstract

The inflammatory response to viral infection is an important component of the antiviral response, a process that involves the activation and proliferation of CD8+ T, CD4+ T, and dendritic cells; thus, viral infection disrupts the immune homeostasis of the organism, leading to an increased release of inflammatory factors. Kikuchi-Fujimoto disease (KFD) is an inflammatory self-limited disorder of unknown etiology, and it is generally believed that the pathogenesis of this disease includes two aspects: viral infection and autoimmune response. Various immune cells, such as CD8+ T lymphocytes, CD4+ T lymphocytes, and CD123+ plasmacytoid dendritic cells, as well as the cytokines they induce and secrete, such as interferons, interleukins, and tumor necrosis factors, play a crucial role in the pathogenesis of KFD. In this article, we present a case study of a young female patient from China who exhibited typical symptoms of lymph node inflammation and fever. The diagnosis of KFD was confirmed through a lymph node biopsy. She presented with elevated ESR, IL-6, and IFN-γ. Viral markers showed elevated IgG and IgM of cytomegalovirus (CMV) and elevated IgG of Epstein-Barr virus (EBV), while changes occurred in the CD4+ T and CD8+ T cell counts. Eventually, the patient achieved disease relief through steroid treatment. Based on these findings, we conducted a comprehensive review of the involvement of viral infection-induced inflammatory response processes and autoimmunity in the pathogenesis of Kikuchi-Fujimoto disease.

Keywords: CD123+ plasmacytoid dendritic cells; CD4+ T lymphocytes; CD8+ T lymphocytes; Kikuchi-Fujimoto disease; immune mechanism; virus-induced inflammation.

Publication types

  • Case Reports
  • Review

MeSH terms

  • Diagnosis, Differential
  • Epstein-Barr Virus Infections* / pathology
  • Female
  • Herpesvirus 4, Human
  • Histiocytic Necrotizing Lymphadenitis* / diagnosis
  • Histiocytic Necrotizing Lymphadenitis* / drug therapy
  • Histiocytic Necrotizing Lymphadenitis* / pathology
  • Humans
  • Immunoglobulin G
  • Lymph Nodes / pathology
  • Lymphadenopathy* / diagnosis
  • Relapsing Fever*

Substances

  • Immunoglobulin G

Grants and funding

The author(s) declare that no financial support was received for the research, authorship, and/or publication of this article.