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Absence of Class A Scavenger Receptor Distinguishes a Phenotype of Tumor Associated Macrophages in Classic Hodgkin's Lymphoma
Author(s) -
Yuan Youzhong,
Holthoff Emily,
Post Jacqueline,
James Jennifer,
Post Ginell R.,
Post Steven R.
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.807.11
Subject(s) - cd68 , cd163 , pathology , lymph node , lymphoma , immunohistochemistry , lymph , macrophage , tumor associated macrophage , cd14 , biology , cancer research , medicine , receptor , tumor microenvironment , in vitro , tumor cells , biochemistry
Tumor‐associated macrophages (TAMs) modulate the development and progression of various cancers. The correlation between adverse clinical prognosis of classic Hodgkin's lymphoma (cHL) patients and the number of TAMs, as defined by CD68, CD163, or CSF1R immunoreactivity in diagnostic lymph node sections indicates that TAMs have an important role in cHL. Although these markers are widely used to identify TAMs, they are detected at all stages of monocyte/macrophage differentiation. In contrast, the Class A scavenger receptor [SR‐A, CD204] is a glycoprotein with an expression profile that is restricted to tissue macrophages. Although SR‐A expression in cHL has not been reported, SR‐A immunoreactivity is inversely correlated with patient prognosis in various carcinomas. To explore the possibility that SR‐A would better correlate with tumor macrophages and therefore be a specific prognostic marker in cHL, lymph node samples from patients with cHL were immunostained with antibodies to CD68 and SR‐A. As additional controls, a subset of cases were also stained with CD14 and CD163. Our results showed robust CD68, CD163, and CD14 stained TAMs in sections from cHL patients, regardless of morphologic subtype. In contrast, most of the TAMs identified with CD68 were negative for SR‐A, with SR‐A staining being limited to macrophages in the fibrous collagenous bands characteristic of nodular sclerosis cHL. Importantly, SR‐A and CD68 staining patterns were similar in recurrent cHL involving the liver, T‐cell‐histiocyte rich lymphoma, and in lymph node metastases of colon carcinoma. The novel finding that, in lymph nodes from cHL patients, SR‐A expression is absent in cells that stain with other monocyte/macrophage markers suggests that these cells may not be fully differentiated macrophages, or that SR‐A is specifically down‐regulated in cHL. In either case, the absence of SR‐A defines a unique phenotype of TAMs in cHL.