The inhibitory collagen receptor LAIR-1 (CD305)

Meyaard, Linde

doi:10.1189/jlb.0907609

Cited by 246 publications

(261 citation statements)

References 53 publications

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“…Underscoring the importance of microenvironmental control in CLL progression, the expression of LAIR-1 in transformed CD5 + B cells is progressively lost with increasing CLL clone aggressiveness ( 54 ). Unfortunately, the lack of LAIR-1 expression in murine B cells ( 48 ) did not allow us to directly test its role in our model. However, LAIR-1 is also expressed by the myeloid component of human lymphoma, and it is lost in CLL, but not DLBCL, in accordance with SPARC expression.…”

Section: Discussionmentioning

confidence: 89%

“…ECM collagens participate in immune cell regulation through the specifi c collagen-binding receptor LAIR-1. LAIR-1 belongs to a class of inhibitory receptors containing immunoreceptor tyrosinebased inhibitory motifs, and their expression characterizes almost all cell types in the immune system ( 48 ). Collagen engagement of LAIR-1 renders immune cells refractory to concomitant activating signals.…”

Section: Discussionmentioning

confidence: 99%

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Defective Stromal Remodeling and Neutrophil Extracellular Traps in Lymphoid Tissues Favor the Transition from Autoimmunity to Lymphoma

et al. 2014

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Altered expression of matricellular proteins can become pathogenic in the presence of persistent perturbations in tissue homeostasis. Here, we show that autoimmunity associated with Fas mutation was exacerbated and transitioned to lymphomagenesis in the absence of SPARC (secreted protein acidic rich in cysteine). The absence of SPARC resulted in defective collagen assembly, with uneven compartmentalization of lymphoid and myeloid populations within secondary lymphoid organs (SLO), and faulty delivery of inhibitory signals from the extracellular matrix. These conditions promoted aberrant interactions between neutrophil extracellular traps and CD5 + B cells, which underwent malignant transformation due to defective apoptosis under the pressure of neutrophil-derived trophic factors and NF-κB activation. Furthermore, this model of defective stromal remodeling during lymphomagenesis correlates with human lymphomas arising in a SPARC-defective environment, which is prototypical of CD5 + B-cell chronic lymphocytic leukemia (CLL). SIGNIFICANCE:These results reveal the importance of stromal remodeling in SLO to accommodate autoimmune lymphoproliferation while preventing lymphomagenesis. Our fi ndings reveal a link between SPARC, collagen deposition, and the engagement of the immune-inhibitory receptor LAIR-1 on neutrophils, neutrophil cell death via NETosis, and the stimulation of CD5 + B-cell proliferation. Moreover, we show that SPARC defi ciency promotes CD5 + B-cell lymphomagenesis and is correlated with CLL in humans. Cancer Discov; 4(1);

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Section: Discussionmentioning

confidence: 89%

Section: Discussionmentioning

confidence: 99%

Defective Stromal Remodeling and Neutrophil Extracellular Traps in Lymphoid Tissues Favor the Transition from Autoimmunity to Lymphoma

et al. 2014

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“…A collagen receptor, the inhibitory leukocyte-associated Ig-like receptor-1 might inhibit the cytotoxic activity of CD8 þ T cells, the cytokine-mediated signal, the differentiation of blood precursor toward DC and induce apoptosis. 13 This is expressed on cells of the immune system including T, B, NK, monocytes and DC that interact with the hydroxyproline of collagen. Hyaluronan could also induce activated T cells to undergo cell death.…”

Section: Discussionmentioning

confidence: 99%

Induction of liver fibrosis in a murine hepatoma model by thioacetamide is associated with enhanced tumor growth and suppressed antitumor immunity

Yang

Chang

Lei

2010

Laboratory Investigation

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Liver cirrhosis and hepatocellular carcinomas are two major causes of morbidity and mortality worldwide, and can synergistically interact to expedite the tumor progression. How fibrosis promotes the hepatoma growth remains completely unexplained. Using an in situ murine hepatoma model together with fibrosis induction by thioacetamide (TAA), the hepatoma growth and the immune factors in the fibrotic liver were analyzed. We found that TAA-fibrosis induction enhanced hepatoma cell growth in the liver and increased the mortality of hepatoma-bearing mice. The tumor-infiltrating CD4 þ or CD8 þ T cells are downregulated by fibrosis induction. The Foxp3 þ regulatory T cells (Treg) cells were induced. We conclude that fibrosis induction causes further immunosuppression, in which Treg cells exert a downregulation effect on the antitumor immunity.

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“…FcRL4 putatively mediates its inhibitory effect on B-cell activation via its cytoplasmic immunoreceptor tyrosine-based inhibitory motif (ITIM). Several other ITIM-containing receptors including CD22, CD72, CD300a, CD305 (LAIR-1), Fγ7RIIB, and CD85j are expressed on B-cells [18][19][20][21][22]24], but the association of these ITIM-bearing receptor expression and B-cell activation in HCV disease remains largely unexamined.…”

Section: Introductionmentioning

confidence: 99%

Peripheral CD27−CD21− B-cells represent an exhausted lymphocyte population in hepatitis C cirrhosis

Doi

Tanoue

Kaplan

2014

Clinical Immunology

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Hepatitis C cirrhosis is associated with a profound disappearance of memory B-cells. We sought to determine if this loss is associated with the expansion of the CD27 − CD21 − tissue-like memory B-cells with features of B-cell exhaustion. To this end, we quantified the frequency of CD27 − CD21 − B-cells in healthy, non-cirrhotic HCV-infected, and cirrhotic patients. We examined the expression of putative inhibitory receptors, the proliferative and immunoglobulin-secreting capacity of CD27/CD21-defined B-cell subsets upon B-cell receptor and/or CD40 stimulation. We found that CD27 − CD21 − B-cells are significantly increased in frequency relative to healthy donors in HCV-infected patients. CD27 − CD21 − B-cells were hypoproliferative relative to naïve and resting memory B-cells upon agonistic stimulation, but retained similar capacity for antibody secretion. Conclusion: CD27 − CD21 − tissue-like memory B-cells with exhausted proliferation circulate at increased frequency in cirrhotic and non-cirrhotic HCV-infected patients. This B-cell subset does not appear anergic, exhibiting immunoglobulin-secreting capacity on CD40 agonism indistinguishable from other CD27/CD21-defined B-cell subsets.

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The inhibitory collagen receptor LAIR-1 (CD305)

Cited by 246 publications

References 53 publications

Defective Stromal Remodeling and Neutrophil Extracellular Traps in Lymphoid Tissues Favor the Transition from Autoimmunity to Lymphoma

Defective Stromal Remodeling and Neutrophil Extracellular Traps in Lymphoid Tissues Favor the Transition from Autoimmunity to Lymphoma

Induction of liver fibrosis in a murine hepatoma model by thioacetamide is associated with enhanced tumor growth and suppressed antitumor immunity

Peripheral CD27−CD21− B-cells represent an exhausted lymphocyte population in hepatitis C cirrhosis

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