Role of CD68 in the tumor immune microenvironment in Hodgkin’s lymphoma

ABSTRACT

Introduction

Despite the high rate of cure in classical Hodgkin Lymphoma (cHL), some patients experienced a refractory disease, sometimes, hardly curable. In the pathogenesis of cHL, Reed Sternberg Cells (HRSC), which represent only less than 1% of tumor cells, are not the only protagonist; in fact, the role of tumor microenvironment is essential in survival, tumor growth, and progression of the disease due to the interaction between immune cells, chemokines, and cytokines.

Areas covered

In this review, the current significant literature was discussed. Many studies demonstrated the role of macrophages CD68+ as ‘protumor’, especially in supporting HRSC survival through cell-to-cell and paracrine interactions. Increased infiltration of CD68 macrophages correlate with a poor prognosis. This review examines the interaction between CD68 macrophages, HRSC and cHL milieu, and the consequent clinical impact, providing an up-do-date portrait of these immune cells with possible translational and therapeutic applications.

Expert opinion

We can suggest that a high baseline CD68 macrophages in cHL patients could contribute to the identification of high-risk patients and help clinicians to choose the best treatment, in the context of refractory disease. A macrophage target strategy in association with chemotherapy or biological therapy could represent a promising approach for future studies and investigations.

KEYWORDS:

• Macrophages
• CD68
• Hodgkin Lymphoma
• prognosis
• immune cells

Article highlights

• The role of microenvironment is crucial in the pathogenesis of Hodgkin Lymphoma

• Macrophages are recruited in neoplasm niche and polarized into tumor associated macrophages.

• Tumor associated CD68+ macrophages are essential for survival, tumor growth, and progression in HL.

• Increased infiltration of CD68+ macrophages are associated with a poor prognosis.

• An efficacy therapy in HL could be against tumor associated macrophages in association with chemo and/or immunotherapy

Declaration of interests

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Reviewer disclosures

Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Additional information

Funding

This paper was not funded.