The role of chemokines in Hodgkin's disease.
Recent studies have analyzed the expression of chemokines in tissues involved by Hodgkin's disease (HD) (1). The data indicate a significant role for chemokine expression in the pathobiology and pathophysiology of HD. In general, HD tissues showed higher levels of chemokine expression than reactive lymphoid hyperplasia (RLH) tissues. There were major differences in chemokine expression among the different HD subtypes. Similar to previous studies in athymic mice that identified a pattern of chemokine response induced by Epstein-Barr virus (EBV)-infected cells, the expression of IP-10, Mig, RANTES, and MIP1-alpha was higher in EBV positive compared to EBV negative HD tissues. In addition, there was a direct correlation of eotaxin expression with tissue eosinophilia. By immunohistochemistry, IP-10 and Mig proteins localized in the malignant Reed-Steinberg (RS) cells and their variants, and to some surrounding inflammatory cells. Eotaxin localized to fibroblasts and smooth muscle of blood vessels. In this review, we discuss the patterns of expression of IP-10, Mig, RANTES, MIP1-alpha, and eotaxin in HD and its subtypes, and the relationship to EBV positivity, LMP1 expression, tissue eosinophilia and T cell infiltration. In addition, we discuss the potential role of chemokines and cytokines in the pathobiology of HD.
Teruya-Feldstein
J
J
Department of Pathology, Memorial Hospital, Memorial Sloan-Kettering Cancer Center, New York, New York 10021, USA. feldstej@mskcc.org
Tosato
G
G
Jaffe
E S
ES
D000818:Animals; D002472:Cell Transformation, Viral; D054413:Chemokine CCL11; D054414:Chemokine CCL17; D018932:Chemokine CCL2 / Q000096:biosynthesis / Q000235:genetics; D054407:Chemokine CCL4; D018946:Chemokine CCL5 / Q000096:biosynthesis / Q000235:genetics; D054357:Chemokine CXCL10; D054370:Chemokine CXCL9; D018925:Chemokines / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology*; D019742:Chemokines, CC / Q000096:biosynthesis / Q000235:genetics; D019743:Chemokines, CXC / Q000096:biosynthesis / Q000235:genetics; D002634:Chemotaxis, Leukocyte; D016207:Cytokines / Q000096:biosynthesis / Q000235:genetics; D004802:Eosinophilia / Q000209:etiology; D020031:Epstein-Barr Virus Infections / Q000235:genetics / Q000378:metabolism; D005260:Female; D020869:Gene Expression Profiling; D015972:Gene Expression Regulation, Neoplastic; D004854:Herpesvirus 4, Human / Q000302:isolation & purification; D006689:Hodgkin Disease / Q000145:classification / Q000235:genetics / Q000378:metabolism* / Q000473:pathology / Q000821:virology; D006801:Humans; D006965:Hyperplasia; D036341:Intercellular Signaling Peptides and Proteins; D018793:Interleukin-13 / Q000096:biosynthesis / Q000235:genetics; D008206:Lymphatic Diseases / Q000378:metabolism; D019402:Macrophage Inflammatory Proteins / Q000096:biosynthesis; D051379:Mice; D008819:Mice, Nude; D016539:Reed-Sternberg Cells / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D016176:T-Lymphocyte Subsets / Q000276:immunology; D014412:Tumor Virus Infections / Q000235:genetics / Q000378:metabolism; D014763:Viral Matrix Proteins / Q000096:biosynthesis / Q000235:genetics
C515456:CCL11 protein, human; C106230:CCL17 protein, human; C080810:CXCL9 protein, human; C515457:Ccl11 protein, mouse; C499538:Ccl17 protein, mouse; D054413:Chemokine CCL11; D054414:Chemokine CCL17; D018932:Chemokine CCL2; D054407:Chemokine CCL4; D018946:Chemokine CCL5; D054357:Chemokine CXCL10; D054370:Chemokine CXCL9; D018925:Chemokines; D019742:Chemokines, CC; D019743:Chemokines, CXC; D016207:Cytokines; C037662:EBV-associated membrane antigen, Epstein-Barr virus; D036341:Intercellular Signaling Peptides and Proteins; D018793:Interleukin-13; D019402:Macrophage Inflammatory Proteins; D014763:Viral Matrix Proteins