Anti-CD40LG monoclonal antibody (CABT-47137MH)

Specifications


Host Species
Mouse
Antibody Isotype
IgG1
Clone
1H4
Species Reactivity
Human
Immunogen
Recombinant human soluble CD154 conjugated to BSA.
Conjugate
Unconjugated

Target


Alternative Names
CD40LG; CD40 ligand; IGM; IMD3; TRAP; gp39
Entrez Gene ID
UniProt ID
P29965

Product Background


Pathway
Adaptive Immune System; Allograft Rejection; Allograft rejection; Asthma; Autoimmune thyroid disease; CD40/CD40L signaling; Calcineurin-regulated NFAT-dependent transcription in lymphocytes; Calcium signaling in the CD4+ TCR pathway;

Citations


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References


Clonal Deletion Established via Invariant NKT Cell Activation and Costimulatory Blockade Requires In Vivo Expansion of Regulatory T Cells

AMERICAN JOURNAL OF TRANSPLANTATION

Authors: Hirai, T.; Ishii, R.; Miyairi, S.; Ikemiyagi, M.; Omoto, K.; Ishii, Y.; Tanabe, K.

Recently, the immune-regulating potential of invariant natural killer T (iNKT) cells has attracted considerable attention. We previously reported that a combination treatment with a liposomal ligand for iNKT cells and an anti-CD154 antibody in a sublethally irradiated murine bone marrow transplant (BMT) model resulted in the establishment of mixed hematopoietic chimerism through in vivo expansion of regulatory T cells (Tregs). Herein, we show the lack of alloreactivity of CD8(+)T cells in chimeras and an early expansion of donor-derived dendritic cells (DCs) in the recipient thymi accompanied by a sequential reduction in the donor-reactive V-T cell receptor repertoire, suggesting a contribution of clonal deletion in this model. Since thymic expansion of donor DCs and the reduction in the donor-reactive T cell repertoire were precluded with Treg depletion, we presumed that Tregs should preform before the establishment of clonal deletion. In contrast, the mice thymectomized before BMT failed to increase the number of Tregs and to establish CD8(+)T cell tolerance, suggesting the presence of mutual dependence between the thymic donor-DCs and Tregs. These results provide new insights into the regulatory mechanisms that actively promote clonal deletion.

Lenalidomide inhibits the proliferation of CLL cells via a cereblon/p21(WAF1/Cip1)-dependent mechanism independent of functional p53

BLOOD

Authors: Fecteau, Jessie-F.; Corral, Laura G.; Ghia, Emanuela M.; Gaidarova, Svetlana; Futalan, Diahnn; Bharati, Ila Sri; Cathers, Brian; Schwaederle, Maria; Cui, Bing; Lopez-Girona, Antonia; Messmer, Davorka; Kipps, Thomas J.

Lenalidomide has demonstrated clinical activity in patients with chronic lymphocytic leukemia (CLL), even though it is not cytotoxic for primary CLL cells in vitro. We examined the direct effect of lenalidomide on CLL-cell proliferation induced by CD154-expressing accessory cells in media containing interleukin-4 and -10. Treatment with lenalidomide significantly inhibited CLL-cell proliferation, an effect that was associated with the p53-independent upregulation of the cyclin-dependent kinase inhibitor, p21(WAF1/Cip1) (p21). Silencing p21 with small interfering RNA impaired the capacity of lenalidomide to inhibit CLL-cell proliferation. Silencing cereblon, a known molecular target of lenalidomide, impaired the capacity of lenalidomide to induce expression of p21, inhibit CD154-induced CLL-cell proliferation, or enhance the degradation of Ikaros family zinc finger proteins 1 and 3. We isolated CLL cells from the blood of patients before and after short-term treatment with low-dose lenalidomide (5 mg per day) and found the leukemia cells were also induced to express p21 in vivo. These results indicate that lenalidomide can directly inhibit proliferation of CLL cells in a cereblon/p21-dependent but p53-independent manner, at concentrations achievable in vivo, potentially contributing to the capacity of this drug to inhibit disease-progression in patients with CLL.

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