TNF-α Contributes to Lymphoid Tissue Disorganization and Germinal Center B Cell Suppression during Intracellular Bacterial Infection
Open accessAbstract
Bacterial, parasitic, and viral infections are well-known causes of lymphoid tissue disorganization, although the factors, both host and/or pathogen derived, that mediate these changes are largely unknown. Ehrlichia muris infection in mice causes a loss of germinal center (GC) B cells that is accompanied by the generation of extrafollicular T-bet+ CD11c+ plasmablasts and IgM memory B cells. We addressed a possible role for TNF-α in this process because this cytokine has been shown to regulate GC development. Ablation of TNF-α during infection resulted in an 8-fold expansion of GL7+ CD38lo CD95+ GC B cells, and a 2.5- and 5-fold expansion of CD138+ plasmablasts and T-bet+ memory cells, respectively. These changes were accompanied by a reduction in splenomegaly, more organized T and B cell zones, and an improved response to Ag challenge. CXCL13, the ligand for CXCR5, was detected at 6-fold higher levels following infection but was much reduced following TNF-α ablation, suggesting that CXCL13 dysregulation also contributes to loss of lymphoid tissue organization. T follicular helper cells, which also underwent expansion in infected TNF-α–deficient mice, may also have contributed to the expansion of T-bet+ B cells, as the latter are known to require T cell help. Our findings contrast with previously described roles for TNF-α in GCs and reveal how host–pathogen interactions can induce profound changes in cytokine and chemokine production that can alter lymphoid tissue organization, GC B cell development, and extrafollicular T-bet+ B cell generation.
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TNFα has been demonstrated to inhibit Tfh differentiation and subsequent germinal center formation.
“One of these studies also noted diminished GC formation that occurred concurrently with high levels of TNFα in lymph node follicles, and TNFα has previously been demonstrated to inhibit Tfh differentiation and subsequent GC formation160.”
From SARS-CoV-2, COVID-19 and the aging immune system (2021) · cites this paper as [160]
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- Authors
- Popescu, M., Cabrera-Martinez, B., & Winslow, G. M.
- Affiliations
- SUNY Upstate Medical University (US)
- Corresponding author
- Winslow, Gary M
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2019-11-01
- Volume
- 203
- Issue
- 9
- Pages
- 2415-2424
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- PMC
- PMC6810925
- OpenAlex
- W2977465092
- Cited by
- 72
- References
- 72
- Citations by year
- 2026: 4 · 2025: 12 · 2024: 10 · 2023: 9 · 2022: 13 · 2021: 14 · 2020: 9 · 2019: 1
- FWCI
- 3.70
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Allergy and Infectious Diseases (R01AI114545)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Immunology and Microbiology › Parasitology › Vector-borne infectious diseases
- Keywords
- TNF-α, germinal center B cells, intracellular bacterial infection, plasmablasts, CXCL13, CXCR5, T follicular helper cells, memory B cells, splenomegaly, host-pathogen interaction, chemokines
- MeSH terms
- Animals, B-Lymphocytes, Bacterial Infections, Immune Tolerance, Immunologic Memory, Lymphoid Tissue, Mice, Inbred C57BL, Tumor Necrosis Factor-alpha, Germinal Center, Mice, Chemokine CXCL13
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