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Levamisole and cellular immunity in rheumatoid arthritis--clinical and laboratory correlates
Studies in a number of laboratories have confirmed a deficiency in lymphocyte PHA mitogen response in patients with rheumatoid arthritis. Improvement in T cell function in these deficient patients had been noted with levamisole treatment. We have also shown clinical improvement associated with reversal of this deficiency during a double-blind controlled study with levamisole. Patients showing good clinical response showed a greater enhancement of T cell function as compared to those patients showing a poor clinical response to levamisole. Clinical responders also showed a significantly greater enhancement with in vitro levamisole added to lymphocyte culture prior to drug treatment than did poor clinical responders. Decreased B cell function, immunoglobulin and autoantibody levels have also been observed with levamisole treatment. These studies may suggest that levamisole is acting by normalizing T cell function with a presumed secondary suppressive effect on B cell autoantibody synthesis.
Studies in a number of laboratories have confirmed a deficiency in lymphocyte PHA mitogen response in patients with rheumatoid arthritis. Improvement in T cell function in these deficient patients had been noted with levamisole treatment. We have also shown clinical improvement associated with reversal of this deficiency during a double-blind controlled study with levamisole. Patients showing good clinical response showed a greater enhancement of T cell function as compared to those patients showing a poor clinical response to levamisole. Clinical responders also showed a significantly greater enhancement with in vitro levamisole added to lymphocyte culture prior to drug treatment than did poor clinical responders. Decreased B cell function, immunoglobulin and autoantibody levels have also been observed with levamisole treatment. These studies may suggest that levamisole is acting by normalizing T cell function with a presumed secondary suppressive effect on B cell autoantibody synthesis.