Dual role of anti-TNF therapy: enhancement of TCR-mediated T cell activation in peripheral blood and inhibition of inflammation in target tissues

Clin Immunol. 2011 May;139(2):164-76. doi: 10.1016/j.clim.2011.01.015. Epub 2011 Jan 31.

Abstract

The impact of anti-TNF therapy on systemic immune responses in patients has not been clearly defined. Here, we examined Th1/Th2/Th17 cytokine expression, activation and proliferation of peripheral T cells from patients with psoriasis and inflammatory bowel disease before and during anti-TNF therapy. In parallel, we calculated the correlation with the clinical response and we monitored cytokine expression in biopsies from inflamed tissues. We evidenced a dual role of TNF-blockade. In peripheral blood, it increased the expression of cytokines such as IL-17, IL-10, and IFN-γ, and enhanced the expression of activation markers and the proliferative response of CD4 T cells to TCR stimulation. By contrast, in biopsies from target tissues, TNF-blockade diminished the expression of Th17/Th1 cytokine and early inflammatory genes. Importantly, the enhanced T cell responses to TCR-stimulation did not impair the clinical response to the therapy and, in responder patients, occurred with the concomitant down-regulation of inflammatory genes in the target tissues.

Publication types

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

MeSH terms

  • Adalimumab
  • Adolescent
  • Adult
  • Aged
  • Aged, 80 and over
  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology
  • Anti-Inflammatory Agents, Non-Steroidal / therapeutic use
  • Antibodies, Monoclonal / pharmacology
  • Antibodies, Monoclonal / therapeutic use
  • Antibodies, Monoclonal, Humanized
  • Antigens, CD / genetics
  • Antigens, CD / metabolism
  • B-Lymphocytes / cytology
  • B-Lymphocytes / metabolism
  • Bacterial Toxins / immunology
  • Blood / drug effects
  • Blood / immunology*
  • Blood / metabolism
  • CD4-Positive T-Lymphocytes / cytology
  • CD4-Positive T-Lymphocytes / drug effects
  • CD4-Positive T-Lymphocytes / immunology
  • CD4-Positive T-Lymphocytes / metabolism
  • Cell Proliferation / drug effects
  • Cytokines / blood
  • Cytokines / genetics
  • Cytokines / metabolism
  • Enterotoxins / immunology
  • Etanercept
  • Female
  • Gene Expression / drug effects
  • Gene Expression / immunology
  • Humans
  • Immunoglobulin G / pharmacology
  • Immunoglobulin G / therapeutic use
  • Inflammation / drug therapy
  • Inflammation / immunology
  • Inflammation / metabolism
  • Inflammatory Bowel Diseases / drug therapy
  • Inflammatory Bowel Diseases / immunology
  • Inflammatory Bowel Diseases / metabolism
  • Infliximab
  • Leukocytes, Mononuclear / drug effects
  • Leukocytes, Mononuclear / immunology
  • Leukocytes, Mononuclear / metabolism
  • Lymphocyte Activation / drug effects*
  • Lymphocyte Activation / immunology
  • Male
  • Middle Aged
  • Psoriasis / drug therapy*
  • Psoriasis / immunology
  • Psoriasis / metabolism
  • Receptors, Antigen, T-Cell / metabolism*
  • Receptors, Tumor Necrosis Factor / therapeutic use
  • Skin / drug effects
  • Skin / immunology*
  • Skin / metabolism
  • Superantigens / immunology
  • T-Lymphocyte Subsets / cytology
  • T-Lymphocyte Subsets / drug effects
  • T-Lymphocyte Subsets / immunology
  • T-Lymphocyte Subsets / metabolism
  • T-Lymphocytes / cytology
  • T-Lymphocytes / drug effects*
  • T-Lymphocytes / immunology
  • T-Lymphocytes / metabolism
  • Treatment Outcome
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors*
  • Tumor Necrosis Factor-alpha / immunology
  • Viral Matrix Proteins / immunology
  • Young Adult

Substances

  • Anti-Inflammatory Agents, Non-Steroidal
  • Antibodies, Monoclonal
  • Antibodies, Monoclonal, Humanized
  • Antigens, CD
  • Bacterial Toxins
  • Cytokines
  • Enterotoxins
  • Immunoglobulin G
  • Receptors, Antigen, T-Cell
  • Receptors, Tumor Necrosis Factor
  • Superantigens
  • Tumor Necrosis Factor-alpha
  • Viral Matrix Proteins
  • enterotoxin F, Staphylococcal
  • Infliximab
  • Adalimumab
  • Etanercept