Macrophages express granzyme B in the lesion areas of atherosclerosis and rheumatoid arthritis

Won-Jung Kim1, Ho Kim, Kyoungho Suk

  • 1Department of Genetic Engineering, School of Life Sciences and Biotechnology, Kyungpook National University, Daegu 702-201, Republic of Korea.

Immunology Letters
|July 3, 2007
PubMed

Insights

Granzyme B, a key immune response enzyme, is found in macrophages within atherosclerotic plaques and rheumatoid arthritis lesions. Its expression in these inflammatory conditions suggests a role in disease progression.

Area of Science:

  • Immunology
  • Cell Biology
  • Pathology

Background:

  • Granzyme B is primarily known for its role in cytotoxic immune responses.
  • Emerging research highlights granzyme B's involvement in extracellular matrix (ECM) remodeling.
  • The expression and function of granzyme B in inflammatory diseases require further elucidation.

Purpose of the Study:

  • To investigate the expression pattern of granzyme B in human atherosclerotic plaques and arthritic joint tissues.
  • To determine if granzyme B is expressed by macrophages in these pathological conditions.
  • To explore the induction of granzyme B expression in macrophages.

Main Methods:

  • Immunohistochemistry and in situ hybridization were used on human atherosclerotic plaques and synovial tissues from rheumatoid arthritis (RA) and osteoarthritis (OA) patients.
  • Human macrophage cell line (THP-1) was utilized to study granzyme B induction.
  • Analysis focused on identifying granzyme B-positive cells and their localization.

Main Results:

  • Granzyme B was detected in macrophages within atherosclerotic plaques, particularly near necrotic cores and shoulder regions.
  • Strong granzyme B expression was observed in macrophages in the lining and perivascular areas of rheumatoid arthritis synovium.
  • No granzyme B-positive cells were found in osteoarthritic synovium.
  • ECM proteins and differentiation agents induced granzyme B expression in THP-1 cells.

Conclusions:

  • Macrophages express granzyme B in human inflammatory diseases like atherosclerosis and rheumatoid arthritis.
  • Granzyme B may contribute to macrophage functions relevant to disease progression in these conditions.
  • The findings expand the known cellular sources and potential roles of granzyme B in pathology.

Related Concept Videos

Chronic Inflammation: Introduction01:12

Chronic Inflammation: Introduction

Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...
Inflammation01:38

Inflammation

Overview
T Cell Types and Functions01:24

T Cell Types and Functions

When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
Phagocytosis of Apoptotic Cells01:17

Phagocytosis of Apoptotic Cells

Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or  immature dendritic cells. Non-professional phagocytes such as  epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes. 
Normal cells contain receptors that prevent them from being recognized by phagocytes.