Association of the numbers of CD163+ cells in lesional skin and serum levels of soluble CD163 with disease progression of cutaneous T cell lymphoma

Sugaya, Makoto; Miyagaki, Tomomitsu; Ohmatsu, Hanako; Suga, Hiraku; Kai, Hiromichi; Kamata, Masahiro; Fujita, Hideki; Asano, Yoshihide; Tada, Yayoi; Kadono, Takafumi; Okochi, Hitoshi; Sato, Shinichi

doi:10.1016/j.jdermsci.2012.07.007

Cited by 91 publications

(90 citation statements)

References 46 publications

(31 reference statements)

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“…40,41 It has been known that during tumor progression, the macrophage phenotype changes from M1 to M2 42 and that tumor-associated macrophages, which prompt tumor progression, exhibit an M2-like phenotype. [43][44][45] An increase in CD163 C cells in MF skin with disease progression has been already reported, 5 and our findings indicate that abundant IL-32 in combination with GM-CSF may increase CD163 C M2 macrophages in MF lesions, thus contributing to tumor progression.…”

Section: Cd68supporting

confidence: 80%

“…MF lesions contain a complex mixture of leukocytes that includes malignant T-cell clones, other T-cell populations, CD163 C macrophages, and a variety of CD11c C myeloid dendritic cell (mDC) subsets. 1,5,6 Ongoing interactions of T-cells with macrophages as well as dendritic cells (DCs) in lesions could lead to chronic T-cell activation or inflammation associated with these lesions.…”

Section: Introductionmentioning

confidence: 99%

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IL-32 induces indoleamine 2,3-dioxygenase⁺CD1c⁺ dendritic cells and indoleamine 2,3-dioxygenase⁺CD163⁺ macrophages: Relevance to mycosis fungoides progression

et al. 2017

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Mycosis fungoides (MF) progresses from patch to tumor stage by expansion of malignant T-cells that fail to be controlled by protective immune mechanisms. In this study, we focused on IL-32, a cytokine, highly expressed in MF lesions. Depending on the other cytokines (IL-4, GM-CSF) present during in vitro culture of healthy volunteers' monocytes, IL-32 increased the maturation of CD11cC myeloid dendritic cells (mDC) and/or CD163 C macrophages, but IL-32 alone showed a clear ability to promote dendritic cell (DC) differentiation from monocytes. DCs matured by IL-32 had the phenotype of skin-resident DCs (CD1c C ), but more importantly, also had high expression of indoleamine 2,3-dioxygenase. The presence of DCs with these markers was demonstrated in MF skin lesions. At a molecular level, indoleamine 2,3-dioxygenase messenger RNA (mRNA) levels in MF lesions were higher than those in healthy volunteers, and there was a high correlation between indoleamine 2,3-dioxygenase and IL-32 expression. In contrast, Foxp3 mRNA levels decreased from patch to tumor stage. Increasing expression of IL-10 across MF lesions was highly correlated with IL-32 and indoleamine 2,3-dioxygenase, but not with Foxp3 expression. Thus, IL-32 could contribute to progressive immune dysregulation in MF by directly fostering development of immunosuppressive mDC or macrophages, possibly in association with IL-10.

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Section: Cd68supporting

confidence: 80%

Section: Introductionmentioning

confidence: 99%

IL-32 induces indoleamine 2,3-dioxygenase⁺CD1c⁺ dendritic cells and indoleamine 2,3-dioxygenase⁺CD163⁺ macrophages: Relevance to mycosis fungoides progression

et al. 2017

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“…M2-type macrophages secrete T-helper type-2 cytokines (interleukin-4, interleukin-13, and transforming growth factor-␤), thus can contribute to an immune-suppressive tumor environment by down-regulating M1 and T-helper type-1 cells and promote tumor-cell survival. 24 These M2 macrophages have been linked to disease progression in CTCL 30 and, in a xenografted CTCL murine model, depletion of M2-like tumor-associated macrophages delayed tumor development. 31 In classic Hodgkin lymphoma, tumorassociated macrophages correlated with resistance to chemotherapy as well as to poor survival outcome.…”

Section: Discussionmentioning

confidence: 99%

Phase II Investigator-Initiated Study of Brentuximab Vedotin in Mycosis Fungoides and Sézary Syndrome With Variable CD30 Expression Level: A Multi-Institution Collaborative Project

Kim

Tavallaee

Sundram

et al. 2015

JCO

241

219

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Purpose In contrast to Hodgkin lymphoma and systemic anaplastic large-cell lymphoma, CD30 expression of malignant lymphocytes in mycosis fungoides (MF) and Sézary syndrome (SS) is quite variable. Clinical activity and safety of brentuximab vedotin, a CD30 targeting antibody-drug conjugate, was evaluated in MF and SS. Tissue and blood biomarkers of clinical response were explored. Patients and Methods In this phase II study, patients with MF or SS with negligible to 100% CD30 expression levels were treated with brentuximab vedotin (1.8 mg/kg) every 3 weeks for a maximum of sixteen doses. The primary end point was overall global response rate. Secondary end points included correlation of tissue CD30 expression level with clinical response, time to response, duration of response, progression-free and event-free survivals, and safety. Results Of the 32 patients enrolled and treated, 30 patients had available efficacy evaluations. Objective global response was observed in 21 (70%) of 30 patients (90% CI, 53% to 83%). CD30 expression assessed by immunohistochemistry was highly variable, with a median CD30max of 13% (range, 0% to 100%). Those with <5% CD30 expression had a lower likelihood of global response than did those with 5% or greater CD30 expression (P < .005). CD163 positive tumor-associated macrophages, many of which coexpress CD30, were abundant in tissue. Peripheral neuropathy was the most common adverse event. Conclusion Brentuximab vedotin demonstrated significant clinical activity in treatment-refractory or advanced MF or SS with a wide range of CD30 expression levels. Additional biomarker studies may help optimize rational design of combination therapies with brentuximab vedotin.

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“…129,130,135 T-cell non-Hodgkin lymphoma Poor prognosis M2-TAMs were related to poor prognosis more closely than were total TAMs. [138][139][140][141][142] TAM: tumor-associated macrophage.…”

Section: Melanomamentioning

confidence: 99%

Role of tumor‐associated macrophages in human malignancies: friend or foe?

Takeya

Komohara

2016

Pathology International

149

146

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Tumor-associated macrophages (TAMs) play a pivotal role in tumor growth in human malignancies. Published studies have analyzed the relationship between TAM infiltration and the prognosis of patients for many human tumors. Most studies reported a positive correlation between TAM density and a poor prognosis. Studies focusing on macrophage phenotypes emphasized the protumor role of M2 anti-inflammatory macrophages in many types of human tumors. However, TAMs influence tumor progression in various ways that depend on differences in tumor sites, histology, and microenvironments. In this review, we summarize the function of TAMs in various human malignancies by reviewing the data provided in studies of TAMs in human malignancies.

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Association of the numbers of CD163+ cells in lesional skin and serum levels of soluble CD163 with disease progression of cutaneous T cell lymphoma

Cited by 91 publications

References 46 publications

IL-32 induces indoleamine 2,3-dioxygenase⁺CD1c⁺ dendritic cells and indoleamine 2,3-dioxygenase⁺CD163⁺ macrophages: Relevance to mycosis fungoides progression

IL-32 induces indoleamine 2,3-dioxygenase⁺CD1c⁺ dendritic cells and indoleamine 2,3-dioxygenase⁺CD163⁺ macrophages: Relevance to mycosis fungoides progression

Phase II Investigator-Initiated Study of Brentuximab Vedotin in Mycosis Fungoides and Sézary Syndrome With Variable CD30 Expression Level: A Multi-Institution Collaborative Project

Role of tumor‐associated macrophages in human malignancies: friend or foe?

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Association of the numbers of CD163+ cells in lesional skin and serum levels of soluble CD163 with disease progression of cutaneous T cell lymphoma

Cited by 91 publications

References 46 publications

IL-32 induces indoleamine 2,3-dioxygenase+CD1c+ dendritic cells and indoleamine 2,3-dioxygenase+CD163+ macrophages: Relevance to mycosis fungoides progression

IL-32 induces indoleamine 2,3-dioxygenase+CD1c+ dendritic cells and indoleamine 2,3-dioxygenase+CD163+ macrophages: Relevance to mycosis fungoides progression

Phase II Investigator-Initiated Study of Brentuximab Vedotin in Mycosis Fungoides and Sézary Syndrome With Variable CD30 Expression Level: A Multi-Institution Collaborative Project

Role of tumor‐associated macrophages in human malignancies: friend or foe?

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IL-32 induces indoleamine 2,3-dioxygenase⁺CD1c⁺ dendritic cells and indoleamine 2,3-dioxygenase⁺CD163⁺ macrophages: Relevance to mycosis fungoides progression

IL-32 induces indoleamine 2,3-dioxygenase⁺CD1c⁺ dendritic cells and indoleamine 2,3-dioxygenase⁺CD163⁺ macrophages: Relevance to mycosis fungoides progression