Anti-Very Late Antigen-1 Monoclonal Antibody Modulates the Development of Secondary Lesion and T-Cell Response in Experimental Arthritis

Ianaro, Angela; Cicala, Carla; Calignano, Antonio; Koteliansky, Victor; Gotwals, Philip J.; Bucci, Mariarosaria; Gerli, Roberto; Santucci, Luca; Fiorucci, Stefano; Cirino, Giuseppe

doi:10.1038/labinvest.3780010

Cited by 31 publications

(18 citation statements)

References 19 publications

(18 reference statements)

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“…Reduced experimental arthritis, reduced contact hypersensitivity (de Fougerolles et al, 2000;Ianaro et al, 2000), reduced DSS colitis (Krieglstein et al, 2002).…”

Section: Inflammation In Knockout Modelsmentioning

confidence: 99%

The integrin–collagen connection – a glue for tissue repair?

Zeltz

Gullberg

2016

Journal of Cell Science

176

126

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There was an error published in J. Cell Sci. 129, 653-664.In Fig. 2A, the fibroblasts were incorrectly labelled. The correct annotation should have been α11 −/− fibroblast (left) and α11 +/+ fibroblast (right). The correct Fig. 2 is shown below. We apologise to the readers for any confusion that this error might have caused. Journal of Cell Science COMMENTARYThe integrin-collagen connection -a glue for tissue repair?Cedric Zeltz and Donald Gullberg* ABSTRACTThe α1β1, α2β1, α10β1 and α11β1 integrins constitute a subset of the integrin family with affinity for GFOGER-like sequences in collagens.Integrins α1β1 and α2β1 were originally identified on a subset of activated T-cells, and have since been found to be expressed on a number of cell types including platelets (α2β1), vascular cells (α1β1, α2β1), epithelial cells (α1β1, α2β1) and fibroblasts (α1β1, α2β1).Integrin α10β1 shows a distribution that is restricted to mesenchymal stem cells and chondrocytes, whereas integrin α11β1 appears restricted to mesenchymal stem cells and subsets of fibroblasts. The bulk of the current literature suggests that collagen-binding integrins only have a limited role in adult connective tissue homeostasis, partly due to a limited availability of cell-binding sites in the mature fibrillar collagen matrices. However, some recent data suggest that, instead, they are more crucial for dynamic connective tissue remodeling events -such as wound healing -where they might act specifically to remodel and restore the tissue architecture. This Commentary discusses the recent development in the field of collagen-binding integrins, their roles in physiological and pathological settings with special emphasis on wound healing, fibrosis and tumor-stroma interactions, and include a discussion of the most recently identified newcomers to this subfamilyintegrins α10β1 and α11β1.

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“…Reduced experimental arthritis, reduced contact hypersensitivity (de Fougerolles et al, 2000;Ianaro et al, 2000), reduced DSS colitis (Krieglstein et al, 2002).…”

Section: Inflammation In Knockout Modelsmentioning

confidence: 99%

The integrin–collagen connection – a glue for tissue repair?

Zeltz

Gullberg

2016

Journal of Cell Science

176

126

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“…59 These results are consistent with other studies demonstrating reduced inflammatory cell accumulation after genetic deletion or antibody blockade of the α 1 β 1 receptor in experimental models of colitis, 60 renal fibrosis, 61 rheumatoid arthritis, and contact-and delayedtype hypersensitivity reactions. 62,63 Taken together, these studies underscore the importance of collagen signaling through the α 1 β 1 integrin in regulating macrophage invasion of tissues during chronic inflammation.…”

Section: Leukocyte Collagen Receptorsmentioning

confidence: 99%

Collagens in the progression and complications of atherosclerosis

et al. 2009

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Collagens constitute a major portion of the extracellular matrix in the atherosclerotic plaque, where they contribute to the strength and integrity of the fibrous cap, and also modulate cellular responses via specific receptors and signaling pathways. This review focuses on the diverse roles that collagens play in atherosclerosis; regulating the infiltration and differentiation of smooth muscle cells and macrophages; controlling matrix remodeling through feedback signaling to proteinases; and influencing the development of atherosclerotic complications such as plaque rupture, aneurysm formation and calcification. Expanding our understanding of the pathways involved in cell-matrix interactions will provide new therapeutic targets and strategies for the diagnosis and treatment of atherosclerosis.

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“…Furthermore, VLA-1/collagen interactions augment T cell receptor-mediated (TCR-mediated) proliferation and cytokine secretion (12,13). Importantly, recent studies in murine models of inflammation show that deleting the α1 integrin gene or blocking the functions of VLA-1 in vivo with mAb's prevents the development of delayed-type hypersensitivity-like (DTHlike) immune responses, including those associated with graft-versus-host disease, adjuvant or Abinduced arthritis, and hapten-induced colitis (14)(15)(16)(17)(18). Notably, in the wild-type untreated animals the majority of T cells (and monocytes) infiltrating the inflamed tissues express VLA-1 (15,18).…”

Section: Introductionmentioning

confidence: 99%

Expression of the α1β1 integrin, VLA-1, marks a distinct subset of human CD4+ memory T cells

Goldstein¹,

Ben‐Horin²,

Li³

et al. 2003

J. Clin. Invest.

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The α1β1 integrin, very late antigen-1 (VLA-1), is a collagen receptor expressed in many CD4 + T cells localizing to inflamed tissues. Here we show that the expression of VLA-1 is a stable marker of a distinct subset of CD4 + memory T cells. Thus, in human peripheral blood lymphocytes (PBLs), approximately 1-4% of the CD4 + T cells express VLA-1, and following T cell receptor activation ex vivo, the percentage of VLA-1 + cells increases within the CD45RO + population. Importantly, the activated VLA-1 + and VLA-1 -cells can be isolated and maintained in culture as phenotypically stable subsets. Functionally, CD4 + memory T cells, operationally defined as the cells that divide rapidly following stimulation with a recall antigen, are highly enriched for VLA-1 + cells. Moreover, depletion of the small fraction of VLA-1 + cells present in CD4 + PBLs prior to stimulation significantly abrogated the proliferative response to recall antigens. Notably, the VLA-1 + cells in fresh CD4 + PBLs are composed of resting CD45RO + /RA -, CCR7 -, CD62L + , CD25 -, and VLA-4 hi cells. Interestingly, this VLA-1 + subset is enriched for Th1-type cells, and Th1-polarizing conditions during T cell activation favor the emergence of VLA-1 + cells. Thus, VLA-1 expression is a stable marker of a unique subset of human memory CD4 + T cells that predominantly differentiates into Th1 cells.

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Anti-Very Late Antigen-1 Monoclonal Antibody Modulates the Development of Secondary Lesion and T-Cell Response in Experimental Arthritis

Cited by 31 publications

References 19 publications

The integrin–collagen connection – a glue for tissue repair?

The integrin–collagen connection – a glue for tissue repair?

Collagens in the progression and complications of atherosclerosis

Expression of the α1β1 integrin, VLA-1, marks a distinct subset of human CD4+ memory T cells

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