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Serum chemokine levels in Hodgkin lymphoma patients: highly increased levels of CCL17 and CCL22
Author(s) -
Niens Marijke,
Visser Lydia,
Nolte Ilja M.,
Van Der Steege Gerrit,
Diepstra Arjan,
Cordano Pablo,
Jarrett Ruth F.,
Te Meerman Gerard J.,
Poppema Sibrand,
Van Den Berg Anke
Publication year - 2008
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.2007.06964.x
Subject(s) - ccl17 , ccl22 , ccr4 , chemokine , immunology , hodgkin lymphoma , lymphoma , single nucleotide polymorphism , medicine , inflammation , biology , chemokine receptor , genotype , gene , biochemistry
Summary Hodgkin lymphoma (HL) is characterized by a minority of neoplastic Hodgkin‐Reed Sternberg (HRS) cells surrounded by a non‐neoplastic reactive infiltrate. As immunological mechanisms appear to be crucial in classical HL pathogenesis, altered serum chemokine levels might be related to disease activity. Serum levels of nine chemokines were examined in 163 untreated HL patients and 334 controls. We investigated single nucleotide polymorphisms (SNPs) for association with serum CCL17 (thymus and activation‐regulated chemokine, TARC) levels and HL susceptibility. Serum CCL17 and CCL22 (macrophage‐derived chemokine, MDC) levels were significantly increased in 82% and 57% of the HL patients. Nodular sclerosis cases showed increased serum CCL17 and CCL22 levels ( P < 0·001) and serum levels were correlated with Ann Arbor stage. Of nine patients with pre‐ and post‐treatment serum samples, the majority showed decreased CCL17 and CCL22 levels after treatment. HRS cells expressed CCL17 and CCL22 in 77% and 75% of 74 cases. Three SNPs showed a trend of increased serum CCL17 levels with minor alleles in controls, but were not associated with HL susceptibility. CCL17 and CCL22 were the only chemokines with increased serum levels in the vast majority of HL patients, which provides further insight into the molecular mechanism(s) leading to infiltrations of reactive lymphocytes in HL.