Publication Date

2017

Document Type

Thesis

Committee Members

Nancy Bigley (Advisor), Barbara Hull (Committee Member), Dawn Wooley (Committee Member)

Degree Name

Master of Science (MS)

Abstract

Macrophages play a key role in both the innate and adaptive immune system responses to foreign materials. Suppressors of cytokine signaling (SOCS) proteins are known as regulators of the immune response through various JAK/STAT pathways. This study examined the roles of SOCS1 and SOCS3 peptide mimetics on the phagocytosis of fluorescently labeled malignant target cell by RAW264.7 murine macrophages. The malignant cells used were Neuro-2a cells, a murine neuroblastoma cell line. A prominent "eat me" signal found in neuroblastoma cells is calreticulin (CRT), which permits macrophages to recognize and then phagocytize the malignant cells. When M1 (pro-inflammatory) polarized macrophages were treated with a SOCS1 peptide mimetic, an increase in phagocytosis was observed, but a SOCS3 peptide mimetic had no effect on phagocytosis. Neither SOCS1 nor 3 peptide mimetics showed a significant effect on the phagocytosis ability of the M2 (anti-inflammatory) polarized macrophages when target cells were stained with carboxyfluorescein succinimidyl ester (CFSE). When target cells were treated with anti-CRT, phagocytosis was decreased by both M1 and M2 polarized macrophages. When M2 macrophages were treated with SOCS3 peptide mimetic and target cells were blocked with anti-CRT, which initiates apoptosis, an increase in phagocytosis compared to unblocked target cells was observed. These results contribute to our continuing understating of the primary functions of M2 macrophages in wound healing and clearance of apoptotic cells. Overall this study provides a mechanism by which SOCS1/3 peptide mimetics can enhance phenotypic specific phagocytosis of pro-inflammatory M1 macrophages and anti-inflammatory M2 macrophages.

Page Count

60

Department or Program

Microbiology and Immunology

Year Degree Awarded

2017

Download


Share

COinS