Anti-TNF treatment blocks the induction of T cell-dependent humoral responses

Ann Rheum Dis. 2013 Jun;72(6):1037-43. doi: 10.1136/annrheumdis-2011-201270. Epub 2012 Sep 11.

Abstract

Objective: Experimental and human data suggest that tumour necrosis factor (TNF) blockade may affect B cell responses, in particular the induction of T cell-dependent (TD) humoral immunity. This study aimed to assess this hypothesis directly in patients with arthritis by analysing longitudinally the effect of TNF blockade on B cell activation and the maturation of humoral responses against TD and T cell-independent vaccines.

Materials and methods: Peripheral blood samples were obtained from 56 spondyloarthritis patients before and after treatment with either non-steroidal anti-inflammatory drug (NSAID) alone or TNF blockers and analysed for B cell activation, plasma cell differentiation, germinal centre versus extra-follicular B cell maturation, and somatic hypermutation. Vaccine responses to hepatitis B and Streptococcus pneumoniae were measured by ELISA.

Results: TNF blockade augmented B cell activation as reflected by the expression of early activation markers, CD40, and costimulatory molecules, without affecting differentiation towards plasmablasts. This was associated with a specific increase of the unswitched fraction of circulating memory B cells and a decreased level of somatic hypermutation in anti-TNF treated patients, indicating an impairment of the germinal centre-dependent B cell maturation. In agreement with these findings, TNF blockade profoundly suppressed the response to the TD vaccination against hepatitis B, whereas the T cell-independent response against pneumococcal polysaccharides was only modestly affected.

Conclusions: These data indicate that TNF blockade severely impedes the induction of primary TD humoral responses, probably by interfering with the germinal centre reaction.

Keywords: Anti-TNF; Autoantibodies; B cells; T Cells; Vaccination.

Publication types

  • Clinical Trial
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adalimumab
  • Adult
  • Antibodies, Monoclonal / therapeutic use
  • Antibodies, Monoclonal, Humanized / therapeutic use
  • Antirheumatic Agents / therapeutic use*
  • B-Lymphocytes / cytology
  • B-Lymphocytes / drug effects*
  • Cell Differentiation / drug effects
  • Cohort Studies
  • Etanercept
  • Female
  • Flow Cytometry
  • Humans
  • Immunity, Humoral / drug effects*
  • Immunoglobulin G / therapeutic use
  • Infliximab
  • Lymphocyte Activation / drug effects*
  • Male
  • Middle Aged
  • Plasma Cells / cytology
  • Plasma Cells / drug effects
  • Receptors, Tumor Necrosis Factor / therapeutic use
  • Spondylarthropathies / drug therapy*
  • Spondylarthropathies / immunology
  • T-Lymphocytes / cytology
  • T-Lymphocytes / drug effects*
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors*

Substances

  • Antibodies, Monoclonal
  • Antibodies, Monoclonal, Humanized
  • Antirheumatic Agents
  • Immunoglobulin G
  • Receptors, Tumor Necrosis Factor
  • Tumor Necrosis Factor-alpha
  • Infliximab
  • Adalimumab
  • Etanercept