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Tumor Necrosis Factor (TNF), a proinflammatory cytokine, contributes significantly to the inflammation seen in Crohn's disease. It exists as soluble TNF and membrane-bound TNF, with actions mediated through TNF receptors (TNFR). TNFR activation leads to the release of proinflammatory cytokines, T-cell activation, collagen production, and leukocyte migration, all contributing to inflammation in Crohn's disease. Anti-TNF monoclonal antibodies, namely infliximab (Remicade), adalimumab (Humira),...
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Related Experiment Video

Updated: May 17, 2026

Dynamic Imaging of Chimeric Antigen Receptor T Cells with [18F]Tetrafluoroborate Positron Emission Tomography/Computed Tomography
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Rituximab combination therapy in relapsing multiple sclerosis.

Anne H Cross1, Robyn S Klein, Laura Piccio

  • 1Department of Neurology, Washington University in St Louis, 660 S Euclid, Campus Box 8111, St Louis, MO 63110, USA.

Therapeutic Advances in Neurological Disorders
|November 10, 2012
PubMed
Summary
This summary is machine-generated.

Rituximab, a B-cell depleting therapy, significantly reduced MRI lesions in relapsing multiple sclerosis (MS) patients unresponsive to other treatments. This therapy also unexpectedly decreased T-cell counts, suggesting B cells have roles beyond antibody production in MS.

Keywords:
B cellsCXCL13T cellschemokinesgadolinium-enhanced magnetic resonance imagingmultiple sclerosisrituximab

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Area of Science:

  • Neuroimmunology
  • Clinical Neurology
  • Immunotherapy

Background:

  • The humoral immune system, involving B cells, plasma cells, and immunoglobulins, is implicated in multiple sclerosis (MS) pathogenesis.
  • B-cell depleting therapies, like rituximab, have emerged as effective treatments for relapsing MS.
  • The role of B cells in MS beyond antibody production remains incompletely understood.

Purpose of the Study:

  • To evaluate rituximab as an add-on therapy in relapsing MS patients with inadequate response to standard injectable disease-modifying therapies (DMTs).
  • To assess the impact of rituximab on MRI-detected disease activity and secondary clinical and laboratory endpoints.

Main Methods:

  • An investigator-initiated phase II clinical trial.
  • Treatment with rituximab in patients with relapsing MS inadequately controlled by standard DMTs.
  • Assessment of MRI gadolinium-enhanced (GdE) lesions, B- and T-cell counts in blood and CSF, chemokine levels, and antibodies to myelin proteins.

Main Results:

  • Rituximab significantly reduced GdE lesions, with 74% of patients being lesion-free post-treatment compared to 26% at baseline (p < 0.0001).
  • No differences in efficacy were observed based on concomitant DMTs.
  • A surprising, significant reduction in T-cell numbers in both peripheral blood and CSF accompanied the B-cell depletion.
  • Declines in CXCL13 and CCL19 chemokine levels were noted, with no significant changes in antibodies against myelin proteins (MBP, MOG).

Conclusions:

  • Rituximab is effective as an add-on therapy for relapsing MS patients with suboptimal response to standard DMTs.
  • B cells may play a role in MS pathogenesis independent of antibody production, potentially through antigen presentation or chemokine/cytokine production.
  • The observed reduction in T cells suggests complex immunomodulatory effects of B-cell depletion in MS.