The number and localization of CD68+ and CD163+ macrophages in different stages of cutaneous melanoma

Salmi, Satu; Siiskonen, Hanna; Sironen, Reijo; Tyynelä-Korhonen, Kristiina; Hirschovits-Gerz, Benjamin; Valkonen, Mari; Auvinen, Päivi; Pasonen‐Seppänen, Sanna

doi:10.1097/cmr.0000000000000522

Cited by 65 publications

(73 citation statements)

References 33 publications

(40 reference statements)

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“…CD206, CD163 and CD204 are useful for M2 detection. Moreover, CD68 is considered a pan‐macrophage marker (Guo et al , ; Gustafson et al , ; Han et al , ; Motomura et al , ; Olesch et al , ; Salmi et al , ; Tan‐Garcia et al , ; Wang et al , ).…”

Section: Introductionmentioning

confidence: 99%

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RACK1 promotes cancer progression by increasing the M2/M1 macrophage ratio via the NF‐κB pathway in oral squamous cell carcinoma

et al. 2020

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Receptor for activated C kinase 1 (RACK1) has been shown to promote oral squamous cell carcinoma (OSCC) progression, and RACK1 expression levels have been negatively correlated with prognosis in patients with OSCC. Here, we investigated the impact of RACK1 OSCC expression on the recruitment and differentiation of tumor‐associated macrophages. High RACK1 expression in OSCC cells correlated with increased M2 macrophage infiltration in tumor samples from a clinical cohort study. Moreover, the combination of RACK1 expression and the M2/M1 ratio could successfully predict prognosis in OSCC. OSCC cells with high RACK1 expression inhibited the migration of THP‐1 cells, promoted M2‐like macrophage polarization in vitro, and increased the proportion of M2‐like macrophages in a xenograft mouse model. Moreover, both M1‐ and M2‐like macrophage polarization‐associated proteins were induced in macrophages cocultured with RACK1‐silenced cell supernatant. A mechanistic study revealed that the expression and secretion of C‐C motif chemokine 2 (CCL2), C‐C motif chemokine 5 (CCL5), interleukin‐6 (IL‐6), and interleukin‐1 (IL‐1) are closely related to RACK1 expression. In addition, blocking nuclear factor‐kappa B (NF‐κB) could promote M2‐like macrophage polarization. These results indicate that RACK1 and the M2/M1 ratio are predictors of a poor prognosis in OSCC. RACK1 promotes M2‐like polarization by regulating NF‐κB and could be used as a potential therapeutic target for antitumor immunity.

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Section: Introductionmentioning

confidence: 99%

“…The most commonly used markers for M1 macrophages are CD11c, CD80 and HLA-DR. CD206, CD163 and CD204 are useful for M2 detection. Moreover, CD68 is considered a pan-macrophage marker (Guo et al, 2018;Gustafson et al, 2015;Han et al, 2016;Motomura et al, 2015;Olesch et al, 2015;Salmi et al, 2018;Tan-Garcia et al, 2017;Wang et al, 2014a).…”

Section: Introductionmentioning

confidence: 99%

RACK1 promotes cancer progression by increasing the M2/M1 macrophage ratio via the NF‐κB pathway in oral squamous cell carcinoma

et al. 2020

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“…TAM are known to produce interleukin (IL)-1β, cyclooxygenase-2, angiotensin, IFN-γ promoting tumorigenesis [69]. These cells can recruit regulatory T cells (Treg) and inhibit effector T cells by secreting IL-10 and expressing PD-L1 [70]. CD68 + TAM in tumor cell nests were described to be associated with a negative prognosis and recurrence in cutaneous melanoma [70].…”

Section: Tumor-associated Macrophages (Tam)mentioning

confidence: 99%

“…These cells can recruit regulatory T cells (Treg) and inhibit effector T cells by secreting IL-10 and expressing PD-L1 [70]. CD68 + TAM in tumor cell nests were described to be associated with a negative prognosis and recurrence in cutaneous melanoma [70]. Furthermore, the ratio of CD8 + T cells to CD68 + macrophages was shown to predict a disease specific survival in melanoma [71].…”

Section: Tumor-associated Macrophages (Tam)mentioning

confidence: 99%

Modern Aspects of Immunotherapy with Checkpoint Inhibitors in Melanoma

Petrova

Arkhypov

Weber

et al. 2020

IJMS

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Although melanoma is one of the most immunogenic tumors, it has an ability to evade anti-tumor immune responses by exploiting tolerance mechanisms, including negative immune checkpoint molecules. The most extensively studied checkpoints represent cytotoxic T lymphocyte-associated protein-4 (CTLA-4) and programmed cell death protein 1 (PD-1). Immune checkpoint inhibitors (ICI), which were broadly applied for melanoma treatment in the past decade, can unleash anti-tumor immune responses and result in melanoma regression. Patients responding to the ICI treatment showed long-lasting remission or disease control status. However, a large group of patients failed to respond to this therapy, indicating the development of resistance mechanisms. Among them are intrinsic tumor properties, the dysfunction of effector cells, and the generation of immunosuppressive tumor microenvironment (TME). This review discusses achievements of ICI treatment in melanoma, reasons for its failure, and promising approaches for overcoming the resistance. These methods include combinations of different ICI with each other, strategies for neutralizing the immunosuppressive TME and combining ICI with other anti-cancer therapies such as radiation, oncolytic viral, or targeted therapy. New therapeutic approaches targeting other immune checkpoint molecules are also discussed.

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“…Macrophages can be divided into two types, MI and M2, and their specific markers on the surface are different. CD68 is a scavenger receptor expressed highly by tissue macrophages and generally considered a pan‐macrophage marker (Pelekanou, Villarroel‐Espindola, Schalper, Pusztai, & Rimm, ; Salmi et al, ; Z.‐G. ZHAO et al, ).…”

Section: Introductionmentioning

confidence: 99%

Morphological reseach on expression of inflammatory mediators in murine models of chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) induced by T2 antigen

et al. 2019

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Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is a common clinical syndrome with unknown aetiology. In this study, we used the T2 peptide in C57BL/6 (B6) mice and Sprague Dawley (SD) rats model during different stages. We sought to understand the role of CD4 + T cells and macrophages in CP/CPPS. A total of 16 B6 mice and 18 SD rats were divided into five groups: B6-naïve (n = 6), B6 model (n = 10), SD-naïve (n = 6), SD-45-day model (n = 6) and SD-56-day model (n = 6). The B6 model group was subcutaneously injected with 0.2 ml of (225μg/ml) T2 peptide on 0 and 14th day and was finally sacrificed on 28th day. The SD-45-and SD-56-day model groups were subcutaneously injected with 1ml of (50 μg/ml) T2 peptide on 0 and 14th day and were finally sacrificed on 45th and 56th day respectively. An equivalent volume of normal saline (NS) solution was injected to the naïve groups and analysed the pain and voiding behaviour. We have calculated the prostate index, H&E staining and immunofluorescence of CD4 + T cells and macrophages (CD68) in each group. T2 peptide immunization in B6 mice and SD rats caused severe prostatitis and cell infiltration, mainly composed of CD4 + T cells and macrophages. The SD-56-day model group showed more severe inflammatory cells infiltration than SD-45-day model group. Moreover, inflammatory cells infiltration and red secretions in B6 model were less than SD model. Expression of CD4 + T cells and macrophages was also consistent with H&E results. These results indicated that different stages of CP/CPPS, inflammatory response, and the inflammation of the rat were stronger than the mouse. Our study suggests that CD4 + T cells and macrophages are key factors in the development of CP/CPPS. K E Y W O R D SCD4 + T cells, CP/CPPS, EAP, macrophages, T2 peptide

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The number and localization of CD68+ and CD163+ macrophages in different stages of cutaneous melanoma

Abstract: Supplemental Digital Content is available in the text.

Cited by 65 publications

References 33 publications

RACK1 promotes cancer progression by increasing the M2/M1 macrophage ratio via the NF‐κB pathway in oral squamous cell carcinoma

RACK1 promotes cancer progression by increasing the M2/M1 macrophage ratio via the NF‐κB pathway in oral squamous cell carcinoma

Modern Aspects of Immunotherapy with Checkpoint Inhibitors in Melanoma

Morphological reseach on expression of inflammatory mediators in murine models of chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) induced by T2 antigen

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