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Published on: June 19, 2012
TCRβ-expressing macrophages induced by a pathogenic murine malaria correlate with parasite burden and enhanced
Miranda S Oakley1, Joanna K Chorazeczewski1, Maya Aleshnick2
1Division of Bacterial, Parasitic, and Allergenic Products, Office of Vaccines Research and Review, Center for Biologics Evaluation and Research, Food and Drug Administration, Silver Spring, MD, United States of America.
Abstract:
Macrophages express a wide array of invariant receptors that facilitate host defense and mediate pathogenesis during pathogen invasion. We report on a novel population of CD11bhighCD14+F4/80+ macrophages that express TCRβ. This population expands dramatically during a Plasmodium berghei ANKA infection and sequesters in the brain during experimental cerebral malaria. Importantly, measurement of TCRβ transcript and protein levels in macrophages in wildtype versus nude and Rag1 knockout mice establishes that the observed expression is not a consequence of passive receptor expression due to phagocytosis or trogocytosis of peripheral T cells or nonspecific antibody staining to an Fc receptor or cross reactive epitope. We also demonstrate that TCRβ on brain sequestered macrophages undergoes productive gene rearrangements and shows preferential Vβ usage. Remarkably, there is a significant correlation in the proportion of macrophages that express TCRβ and peripheral parasitemia. In addition, presence of TCRβ on the macrophage also correlates with a significant increase (1.9 fold) in the phagocytosis of parasitized erythrocytes. By transcriptional profiling, we identify a novel set of genes and pathways that associate with TCRβ expression by the macrophage. Expansion of TCRβ-expressing macrophages points towards a convergence of the innate and adaptive immune responses where both arms of the immune system cooperate to modulate the host response to malaria and possibly other infections.
Insights
A novel macrophage population expressing T cell receptor beta (TCRβ) expands during malaria infection, migrating to the brain. These TCRβ-expressing macrophages enhance the phagocytosis of infected red blood cells, suggesting immune response convergence.
Area of Science:
- Immunology
- Infectious Diseases
- Cell Biology
Background:
- Macrophages are key immune cells involved in host defense and disease pathogenesis.
- Invariant receptors on macrophages mediate pathogen recognition and immune responses.
- Experimental cerebral malaria (ECM) is a severe complication of Plasmodium berghei ANKA infection.
Purpose of the Study:
- To identify and characterize a novel macrophage population expressing T cell receptor beta (TCRβ).
- To investigate the role of TCRβ-expressing macrophages in Plasmodium berghei ANKA infection and experimental cerebral malaria.
- To explore the functional consequences and molecular mechanisms associated with TCRβ expression on macrophages.
Main Methods:
- Flow cytometry to identify and quantify macrophage populations (CD11bhighCD14+F4/80+).
- Gene expression analysis (transcript and protein levels) of TCRβ in macrophages from wildtype and knockout mice (nude, Rag1).
- Analysis of TCRβ gene rearrangements and Vβ usage.
- Assessment of phagocytic activity of macrophages towards parasitized erythrocytes.
- Transcriptional profiling to identify associated genes and pathways.
Main Results:
- A novel population of CD11bhighCD14+F4/80+ macrophages expressing TCRβ was identified.
- This TCRβ-macrophage population significantly expands during Plasmodium berghei ANKA infection and accumulates in the brain during ECM.
- TCRβ expression on macrophages is intrinsic, not due to passive uptake or non-specific staining, and involves productive gene rearrangements.
- TCRβ-macrophage proportion correlates with parasitemia and enhances phagocytosis of infected erythrocytes by 1.9-fold.
- Transcriptional profiling revealed novel genes and pathways associated with TCRβ expression in macrophages.
Conclusions:
- Expansion of TCRβ-expressing macrophages represents a significant convergence of innate and adaptive immunity during malaria.
- These macrophages play a crucial role in modulating the host response to Plasmodium infection.
- The findings suggest a potential new therapeutic target for malaria and other infectious diseases.
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