Human alveolar macrophages present antigen ineffectively due to defective expression of B7 costimulatory cell surface molecules.

C J Chelen; Y Fang; G J Freeman; H Secrist; J D Marshall; P T Hwang; L R Frankel; R H DeKruyff; D T Umetsu

doi:10.1172/JCI117796

Division of Allergy, Immunology, and Respiratory Medicine, Stanford University, Lucile Salter Packard Children's Hospital, California 94305-5119.

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Division of Allergy, Immunology, and Respiratory Medicine, Stanford University, Lucile Salter Packard Children's Hospital, California 94305-5119.

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Division of Allergy, Immunology, and Respiratory Medicine, Stanford University, Lucile Salter Packard Children's Hospital, California 94305-5119.

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Division of Allergy, Immunology, and Respiratory Medicine, Stanford University, Lucile Salter Packard Children's Hospital, California 94305-5119.

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Division of Allergy, Immunology, and Respiratory Medicine, Stanford University, Lucile Salter Packard Children's Hospital, California 94305-5119.

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Division of Allergy, Immunology, and Respiratory Medicine, Stanford University, Lucile Salter Packard Children's Hospital, California 94305-5119.

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Division of Allergy, Immunology, and Respiratory Medicine, Stanford University, Lucile Salter Packard Children's Hospital, California 94305-5119.

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Division of Allergy, Immunology, and Respiratory Medicine, Stanford University, Lucile Salter Packard Children's Hospital, California 94305-5119.

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Division of Allergy, Immunology, and Respiratory Medicine, Stanford University, Lucile Salter Packard Children's Hospital, California 94305-5119.

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Published in Volume 95, Issue 3 on March 1, 1995
J Clin Invest. 1995;95(3):1415–1421. https://doi.org/10.1172/JCI117796.
© 1995 The American Society for Clinical Investigation

Published March 1, 1995 - Version history

Alveolar macrophages, resident phagocytic cells in the lung that derive from peripheral blood monocytes, are paradoxically ineffective in presenting antigen to T cells. We found that antigen presentation by alveolar macrophages could be restored by the addition of anti-CD28 mAb to cultures of T cells and macrophages, indicating that costimulation by alveolar macrophages via the CD28 pathway was defective. In addition, we found that alveolar macrophages activated with IFN-gamma failed to express B7-1 or B7-2 antigens, which normally ligate CD28 on T cells and provide a costimulatory signal required for the activation of T cells. These observations are the first to demonstrate the inability of a "professional" antigen-presenting cell type to effectively express the costimulatory molecules B7-1 and B7-2. Inasmuch as immune reactions within the lung are inevitably associated with inflammatory injury to pulmonary tissue, these observations suggest that reduced expression of B7-1 and B7-2 by alveolar macrophages may be advantageous, as a critical mechanism involved in the induction of peripheral tolerance to the abundance of antigens to which mucosal tissues are continuously exposed.

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Human alveolar macrophages present antigen ineffectively due to defective expression of B7 costimulatory cell surface molecules.

C J Chelen, Y Fang, G J Freeman, H Secrist, J D Marshall, P T Hwang, L R Frankel, R H DeKruyff, and D T Umetsu

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Human alveolar macrophages present antigen ineffectively due to defective expression of B7 costimulatory cell surface molecules.

C J Chelen, Y Fang, G J Freeman, H Secrist, J D Marshall, P T Hwang, L R Frankel, R H DeKruyff, and D T Umetsu

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