RAG-1-deficient mice have no mature B and T lymphocytes

Mombaerts, Peter; Iacomini, John; Johnson, Randall S.; Herrup, Karl; Tonegawa, Susumu; Papaioannou, Virginia E.

doi:10.1016/0092-8674(92)90030-g

Cited by 2,628 publications

(1,882 citation statements)

References 41 publications

Supporting

Mentioning

1,823

Contrasting

Unclassified

Order By: Relevance

“…Antibodies to AChR are ultimately responsible for the block at the neuromuscular junction that leads to muscular weakness. It will be important to address next whether CCL2 may be a specific therapeutic target to modulate clinical MG. Mice C57BL/6 (B6) mice deficient of MCP-1 (MCP-1 -/-) [11], IL-6 (IL-6 -/-), IFN (IFN-c -/-) and RAG (RAG-c -/-) [30] were purchased from The Jackson Laboratory (Bar Harbor, ME). IL-17 -/-mice were provided by Dr. Yoichiro Iwakura [5].…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

CCL2 recruitment of IL‐6‐producing CD11b⁺ monocytes to the draining lymph nodes during the initiation of Th17‐dependent B cell‐mediated autoimmunity

et al. 2008

View full text Add to dashboard Cite

The development and function of Th17 cells are influenced in part by the cytokines TGF-b, IL-23 and IL-6, but the mechanisms that govern recruitment and activity of Th17 cells during initiation of autoimmunity remain poorly defined. We show here that the development of autoreactive Th17 cells in secondary lymphoid organs in experimental autoimmune myasthenia gravis -an animal model of human myasthenia gravis -is modulated by IL-6-producing CD11b + cells via the CC chemokine ligand 2 (CCL2). Notably, acetylcholine receptor (AChR)-reactive Th17 cells provide help for the B cells to produce anti-AChR antibodies, which are responsible for the impairment of the neuromuscular transmission that contributes to the clinical manifestations of autoimmunity, as indicated by a lack of disease induction in IL-17-deficient mice. Thus, Th17 cells can promote humoral autoimmunity via a novel mechanism that involves CCL2.

show abstract

Section: Discussionmentioning

confidence: 99%

“…We isolated CD4 + cells from control mice and CCL2 -/-for transfer into RAG1 -/-deficient mice (which are devoid of intrinsic T and B cells) [30]. The transferred CD4 + cells preferentially produced Th17 in control mice but not in CCL2 -/-mice.…”

Section: Autoreactive Th17 Cells Drive Igg2b Antibody Response In Vivomentioning

confidence: 99%

CCL2 recruitment of IL‐6‐producing CD11b⁺ monocytes to the draining lymph nodes during the initiation of Th17‐dependent B cell‐mediated autoimmunity

et al. 2008

View full text Add to dashboard Cite

show abstract

“…Surgeries were performed on six to twelve week-old FVB/N, ND4 (Harlan BioProducts, Indianapolis, IN), C57Bl/6, BALB/c, or Rag-1 −/− mice (Jackson Laboratory, Bar Harbor, ME) that lack mature lymphocytes (13). FVB/N, C57Bl/6 and BABL/c mice were chosen since they are commonly used inbred strains while ND4 mice were chosen since they are a commonly used outbred strain.…”

Section: Pneumonia Modelmentioning

confidence: 99%

Neutrophil Depletion Causes a Fatal Defect in Murine Pulmonary Staphylococcus aureus clearance

Robertson

Perrone

McConnell

et al. 2008

Journal of Surgical Research

View full text Add to dashboard Cite

show abstract

“…C57BL/6J (normal B6) mice, B6 MHC-II -/-(A § -/-or A g -/-) mice [40][41][42] and C57BL/6J-Rag1 tm1Mom (RAG1 -/-) mice [43] (Jackson Labs; stock no. 2216) were used.…”

Section: Micementioning

confidence: 99%

MHC class II‐independent CD25⁺ CD4⁺ CD8α β⁺ α β T cells attenuate CD4⁺ T cell‐induced transfer colitis

2004

View full text Add to dashboard Cite

CD4 + § g T cell populations that develop in mice deficient in MHC class II (through 'knockout' of either the A § , or the A g chain of the I-A b molecule) comprise a major 'single-positive' (SP) CD4 + CD8 -subset (60-90%) and a minor 'double-positive' (DP) CD4 + CD8 § g + subset (10-40%). Many DP T cells found in spleen, mesenteric lymph nodes (MLN) and colonic lamina propria (cLP) express CD25, CD103 and Foxp3. Adoptive transfer of SP but not DP T cells from A § -/-or A g -/-B6 mice into congenic RAG -/-hosts induces colitis. Transfer of SP T cells repopulates the host with only SP T cells; transfer of DP T cells repopulates the host with DP and SP T cells. Anti-CD25 antibody treatment of mice transplanted with DP T cells induces severe, lethal colitis; anti-CD25 antibody treatment of mice transplanted with SP T cells further aggravates the course of severe colitis. Hence, regulatory CD25 + T cells within (or developing from) the DP T cell population of MHC class II-deficient mice control the colitogenic potential of CD25 -CD4 + T cells.

show abstract

RAG-1-deficient mice have no mature B and T lymphocytes

Cited by 2,628 publications

References 41 publications

CCL2 recruitment of IL‐6‐producing CD11b⁺ monocytes to the draining lymph nodes during the initiation of Th17‐dependent B cell‐mediated autoimmunity

CCL2 recruitment of IL‐6‐producing CD11b⁺ monocytes to the draining lymph nodes during the initiation of Th17‐dependent B cell‐mediated autoimmunity

Neutrophil Depletion Causes a Fatal Defect in Murine Pulmonary Staphylococcus aureus clearance

MHC class II‐independent CD25⁺ CD4⁺ CD8α β⁺ α β T cells attenuate CD4⁺ T cell‐induced transfer colitis

Contact Info

Product

Resources

About

RAG-1-deficient mice have no mature B and T lymphocytes

Cited by 2,628 publications

References 41 publications

CCL2 recruitment of IL‐6‐producing CD11b+ monocytes to the draining lymph nodes during the initiation of Th17‐dependent B cell‐mediated autoimmunity

CCL2 recruitment of IL‐6‐producing CD11b+ monocytes to the draining lymph nodes during the initiation of Th17‐dependent B cell‐mediated autoimmunity

Neutrophil Depletion Causes a Fatal Defect in Murine Pulmonary Staphylococcus aureus clearance

MHC class II‐independent CD25+ CD4+ CD8α β+ α β T cells attenuate CD4+ T cell‐induced transfer colitis

Contact Info

Product

Resources

About

CCL2 recruitment of IL‐6‐producing CD11b⁺ monocytes to the draining lymph nodes during the initiation of Th17‐dependent B cell‐mediated autoimmunity

CCL2 recruitment of IL‐6‐producing CD11b⁺ monocytes to the draining lymph nodes during the initiation of Th17‐dependent B cell‐mediated autoimmunity

MHC class II‐independent CD25⁺ CD4⁺ CD8α β⁺ α β T cells attenuate CD4⁺ T cell‐induced transfer colitis