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Dale E. McFarlin, MD; Henry F. McFarland, MD

Arch Neurol. 1976;33(6):395-398.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

At the present time, investigation of the histocompatibility (HL-A) background in human diseases is being extensively pursued. The popularity of this approach is exemplified by the four articles dealing with studies of multiple sclerosis (MS) and HL-A antigens in this issue of the ARCHIVES. Zeal for investigation of this type comes from the view that studies of histocompatibility may provide insight into the genetic predisposition and pathogenesis of human disease.

The concept of histocompatibility was initially derived from transplantation studies. Tissue or skin from one individual grafted on to another individual is rejected through an immune response. The antigens on the transplanted tissue evoking graft rejection are called histocompatibility antigens. Breeding studies in animals, particularly mice, have established that histocompatibility is genetically controlled; thus, specific proteins on the cell surface are specified by the genetic composition of the individual. Further exploration of this phenomenon has revealed that specific regions of . . . [Full Text PDF of this Article]

Author Affiliations
Neuroimmunology Branch; National Institute of Neurological and Communicative Disorders and Stroke; National Institutes of Health Bethesda, MD 20014

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