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When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
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Rheumatic heart disease (RHD) management can be divided into two main strategies: prevention and long-term management.Primary PreventionPrimary prevention focuses on timely diagnosis and management of group A streptococcal pharyngitis to prevent acute rheumatic fever. The most widely used antibiotic for treating this condition is intramuscular benzathine penicillin G.Acute Rheumatic Fever TreatmentThe primary treatment goal for a patient diagnosed with acute rheumatic fever is to suppress the...
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Rheumatic heart disease or RHD is a chronic condition that results from rheumatic fever, causing permanent damage to the heart valves.Etiology and Risk FactorsIt primarily arises from rheumatic fever, an inflammatory disease that can develop after untreated or inadequately treated group A streptococcal (GAS) pharyngitis. Streptococcus spreads through direct contact with oral or respiratory secretions. While the bacteria are the causative agents, factors like malnutrition, overcrowding, poor...
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The key clinical manifestations of Rheumatic heart disease (RHD) include several distinct cardiac symptoms.Carditis, a hallmark of acute rheumatic fever, involves inflammation of the heart's endocardium, myocardium, and pericardium. Chronic RHD often results from recurrent episodes of carditis. Its symptoms include the following:Murmurs are caused by valvular damage, especially to the mitral and aortic valves. Mitral stenosis or regurgitation is common, with characteristic heart murmurs...
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AssessmentA comprehensive assessment is essential in managing a patient with rheumatic heart disease (RHD). Begin with obtaining a detailed medical history, including recent streptococcal infections, a history of rheumatic fever, or previously diagnosed rheumatic heart disease. Assess the patient for symptoms such as fever, chest pain, widespread joint pain (arthralgia), tachycardia, pericardial friction rub, muffled heart sounds, heart murmurs, peripheral edema, subcutaneous nodules, and...
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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...
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Cellular therapies for rheumatic disease.

Fotios Koumpouras1, Roberto Caricchio2

  • 1Section of Rheumatology Allergy and Immunology, Department of Medicine, Yale School of Medicine, New Haven, Connecticut.

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Summary
This summary is machine-generated.

Chimeric antigen receptor (CAR) T-cell therapy shows promise for treating autoimmune rheumatic diseases like lupus, potentially leading to drug-free remission. Further research is needed to optimize trial design and ensure safe, equitable access to these transformative treatments.

Keywords:
autoimmune rheumatic diseasebi-specific t-cell engagerscellular therapieschimeric antigen receptor Tsystemic lupus erythematosus

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Area of Science:

  • Immunology
  • Rheumatology
  • Cellular Therapy

Background:

  • Cellular therapies, especially CAR T-cells, are emerging as viable treatments for autoimmune rheumatic diseases.
  • Conventional therapies often fall short for conditions like systemic lupus erythematosus (SLE), idiopathic inflammatory myopathies (IIM), and systemic sclerosis (SSc).

Purpose of the Study:

  • To review the rationale, clinical experience, safety, and future directions of cellular therapies in rheumatology.
  • To focus on the efficacy, safety, and immune reset potential of these therapies in autoimmune rheumatic diseases.

Main Methods:

  • Review of current clinical data and studies on CAR T-cell therapy in rheumatic diseases.
  • Analysis of safety profiles, including cytokine release syndrome (CRS) and immune effector cell-associated neurotoxicity syndrome (ICANS).

Main Results:

  • CD19-directed CAR T-cells demonstrate significant B-cell depletion and high rates of drug-free remission in refractory SLE.
  • Promising responses observed in SSc and IIM, with manageable toxicities (low-grade CRS, rare ICANS).
  • Evidence of "immune reset" and the development of allogeneic and novel CAR platforms (CAR-NK, RNA CARs).

Conclusions:

  • Cellular therapies offer transformative potential for severe, refractory autoimmune rheumatic diseases.
  • Emphasizes the need for rigorous trial design, long-term safety monitoring, and equitable patient access.