This Article Full Text Full Text (PDF) Purchase Article View Shopping Cart Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kuwata, K. Articles by Naito, M. Search for Related Content PubMed PubMed Citation Articles by Kuwata, K. Articles by Naito, M.

(American Journal of Pathology. 2003;162:837-847.)
© 2003 American Society for Investigative Pathology

AIM Inhibits Apoptosis of T Cells and NKT Cells in Corynebacterium-Induced Granuloma Formation in Mice

Kazuhisa Kuwata^*, Hisami Watanabe, Shu-Ying Jiang^*, Takashi Yamamoto^*, Chikako Tomiyama-Miyaji, Toru Abo, Toru Miyazaki^¶ and Makoto Naito^*

From the Department of Cellular Function, Division of Cellular and Molecular Pathology^* and the Division of Immunology and Medical Zoology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan; the Department of Medical Technology, School of Health Sciences, Faculty of Medicine, Niigata University, Niigata, Japan; the Division of Cellular and Molecular Immunology, Center of Molecular Biosciences, University of the Ryukyus, Nishihara, Okinawa, Japan; and the Center for Immunology, ^¶ The University of Texas Southwestern Medical Center, Dallas, Texas

Apoptosis inhibitor expressed by macrophages (AIM) inhibits apoptosis of CD4⁺CD8⁺ (CD4/CD8) double-positive thymocytes, and supports the viability of these cells on the thymic selection. However, pleiotropic functions of AIM have been suggested. In this study, heat-killed Corynebacterium parvum (C. parvum) was injected into mice carrying the homozygous mutation (AIM^-/-) and wild-type (AIM^+/+) mice, to investigate the role of AIM in the formation of hepatic granulomas. In AIM^-/- mice, the size and the number of hepatic granulomas were larger, and the resorption of granulomas was more delayed than in AIM^+/+ mice. The production of interleukin-12 was more prominent in AIM^-/- mice than in AIM^+/+ mice. In the liver of AIM^+/+ mice, expression of AIM messenger ribonucleic acid (mRNA) increased after C. parvum injection. In situ hybridization demonstrated that AIM mRNA was expressed in Kupffer cells and exudate macrophages in the liver, especially in granulomas. Larger numbers of T cells and natural killer T (NKT) cells underwent apoptosis in the granulomas of AIM^-/- mice, suggesting that AIM prevents apoptosis of NKT cells and T cells in C. parvum-induced inflammation. Recombinant AIM (rAIM) protein significantly inhibited apoptosis of NKT cells and T cells obtained from C. parvum-stimulated livers in vitro. These results indicate that AIM functions to induce resistance to apoptosis within NKT cells and T cells, and supports the host defense in granulomatous inflammation.

This article has been cited by other articles:

				P. Qu, H. Du, Y. Li, and C. Yan Myeloid-Specific Expression of Api6/AIM/Sp{alpha} Induces Systemic Inflammation and Adenocarcinoma in the Lung J. Immunol., February 1, 2009; 182(3): 1648 - 1659. [Abstract] [Full Text] [PDF]

				O. A. Alexeyev, I. Marklund, B. Shannon, I. Golovleva, J. Olsson, C. Andersson, I. Eriksson, R. Cohen, and F. Elgh Direct Visualization of Propionibacterium acnes in Prostate Tissue by Multicolor Fluorescent In Situ Hybridization Assay J. Clin. Microbiol., November 1, 2007; 45(11): 3721 - 3728. [Abstract] [Full Text] [PDF]

				X. Lian, C. Yan, Y. Qin, L. Knox, T. Li, and H. Du Neutral Lipids and Peroxisome Proliferator-Activated Receptor-{gamma} Control Pulmonary Gene Expression and Inflammation-Triggered Pathogenesis in Lysosomal Acid Lipase Knockout Mice Am. J. Pathol., September 1, 2005; 167(3): 813 - 821. [Abstract] [Full Text] [PDF]