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Angioimmunoblastic T-cell lymphoma (AITL) is a peripheral T-cell lymphoma characterized by systemic disease with polymorphous infiltrate including macrophages. Although many studies of tumor-associated macrophage (TAM) populations in various malignant tumors have been published, only a few have dealt with activation of macrophage phenotypes such as M1 and M2 in tumor tissue. Because M2 macrophages highly express CD163, we suspected that CD163 may be a useful marker for identification of activation of macrophage phenotypes in AITL. We performed a retrospective study of immunohistochemical expression using two markers for macrophages [CD68 (PG-M1), CD163] and of the correlation of these expressions with overall survival of 42 AITL patients. The number of CD68-positive cells in AITL tissues did not correlate with overall survival (P= 0.59), whereas the number of CD163-positive cells and overall survival correlated to some extent (P= 0.08). Meanwhile, a higher ratio of CD163-positive to CD68-positive cells in AITL significantly correlated with worse overall survival (P= 0.036). Considering that this ratio reflects the proportion of macrophages polarized to the M2 phenotype, our findings indicate that activation of macrophages towards the M2 phenotype correlates with worse prognosis. Our findings indicate that the ratio of M2 macrophages expressed may be a useful marker for prognosis of AITL.

Macrophage polarization is divided into M1 and M2 type based on membrane receptors, cytokines, and chemokines. M1 expresses CD80, interleukin (IL)-6, IL-12, and chemokine receptor (CCR)7, while M2 expresses CD163, IL10, and chemokine ligand (CCL)22. The aim of the present study was to identify the properties of infiltrating tissue macrophages in histiocytic necrotizing lymphadenitis (HNL). Twenty patients with HNL were studied, and immunohistochemistry for CD68 (KP1), CD163, CCL22, CCR7, and CD123 was done, along with myeloperoxidase (MPO). To evaluate the phenotypes of tissue macrophages in HNL, the number of cells stained positively for CD163, CCL22, CCR7, CD123 and MPO concurrently with CD68 was counted, and the ratio was calculated for each antibody to CD68+ cells. There was a high rate of co-expression for CD163 (median, 78%) or CCL22 (80%) and a low rate for CCR7 (5%) in CD68+ cells. It is therefore conceivable that infiltration by M2 macrophages is dominant in HNL. Furthermore, some CD68+ tissue macrophages in HNL co-express MPO or CD123 (range, 5-80%; median, 23% and 40%, respectively). It is suggested that these characteristic tissue macrophages may be associated with the pathogenesis of HNL and that M2 macrophages may infiltrate to repair the lymphoid tissue injured by cytotoxic T cells in HNL.