CXCL13 Antibody (Rabbit mAb) [E12F15]

Application: Reactivity: Mouse

Usage Information

Dilution
IHC1:500

Application
IHC

Reactivity
Mouse

Source
Rabbit Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW
13 kDa

Positive Control	Mouse spleen tissue
Negative Control	Mouse cerebral cortex tissue

Datasheet & SDS

Biological Description

Specificity
CXCL13 Antibody (Rabbit mAb) [E12F15] detects endogenous levels of total CXCL13 protein.

Clone
E12F15

Synonym(s)
Blc, Scyb13, Cxcl13, C-X-C motif chemokine 13, B lymphocyte chemoattractant, CXC chemokine BLC, Small-inducible cytokine B13

Background
CXCL13, originally identified as B-cell-attracting chemokine 1 (BCA-1), belongs to the CXC subfamily of chemokines and acts through a single cognate receptor, CXCR5, forming a dedicated ligand-receptor axis that governs the architecture of secondary lymphoid organs (SLOs) such as lymph nodes, spleen, and Peyer's patches.CXCL13 and its receptor, CXCR5, make crucial contributions to this process by triggering intracellular signaling cascades in malignant cells and modulating the complex tumor microenvironment in an autocrine or paracrine fashion. Under physiological conditions, the same axis directs naive B cells and CXCR5-expressing T follicular helper (Tfh) cells toward B-cell follicles. CXCL13 is secreted by follicular helper T cells, follicular dendritic cells, and marginal reticular cells, and it recruits peripheral CXCR5-positive B cells into the B-cell zone or germinal center through high endothelial venules, where CXCL13 enhances follicle development and sustains secondary lymphoid organ homeostasis through a positive-feedback loop with B cells and follicular dendritic cells. Ligand engagement dissociates the receptor-coupled heterotrimeric G protein into Gα and Gβγ subunits, initiating distinct downstream cascades that translate the chemokine gradient into directional migration and cytoskeletal reorganization. CXCR5 enables B cells and Tfh cells to follow CXCL13 gradients toward B-cell follicles, establishing the spatial proximity required for productive T cell–B cell interaction, and naive T cells primed by dendritic cells generate CXCR5-positive pre-Tfh cells that migrate along CXCL13 gradients toward follicles, where interactions with cognate B cells license their entry and maturation into fully programmed B-cell helpers. This positioning underlies the generation of high-affinity antibody responses, since Tfh cells are essential contributors to B-cell proliferation, differentiation, and high-affinity antibody synthesis and are required for germinal center formation and maintenance. The axis extends adaptive immune organization into non-lymphoid tissue: CXCL13/CXCR5 activities organize and shape adaptive B-cell-related immune responses outside secondary lymphoid organs through the formation of ectopic lymphoid structures in inflamed tissues, including the central nervous system, and correspondingly, CXCL13 is proposed to recruit B cells to the cerebrospinal fluid during neuroinflammation. In malignancy, receptor engagement reshapes the tumor microenvironment through recruitment of both effector and suppressive populations, so that the CXCL13/CXCR5 axis has a dominant role in B-cell recruitment and tertiary lymphoid structure formation, activating immune responses against some tumors, while in most cancer types the same axis mediates pro-neoplastic immune reactions by recruiting suppressive immune cells into tumor tissue. Disruption of the axis at the developmental level produces measurable structural consequences, as CXCL13/CXCR5-deficient mice show incomplete maturation of lymph nodes. In contrast, overexpression of the pathway causes ectopic lymphoid structures to develop in non-lymphoid tissue.

Background

CXCL13, originally identified as B-cell-attracting chemokine 1 (BCA-1), belongs to the CXC subfamily of chemokines and acts through a single cognate receptor, CXCR5, forming a dedicated ligand-receptor axis that governs the architecture of secondary lymphoid organs (SLOs) such as lymph nodes, spleen, and Peyer's patches.CXCL13 and its receptor, CXCR5, make crucial contributions to this process by triggering intracellular signaling cascades in malignant cells and modulating the complex tumor microenvironment in an autocrine or paracrine fashion. Under physiological conditions, the same axis directs naive B cells and CXCR5-expressing T follicular helper (Tfh) cells toward B-cell follicles. CXCL13 is secreted by follicular helper T cells, follicular dendritic cells, and marginal reticular cells, and it recruits peripheral CXCR5-positive B cells into the B-cell zone or germinal center through high endothelial venules, where CXCL13 enhances follicle development and sustains secondary lymphoid organ homeostasis through a positive-feedback loop with B cells and follicular dendritic cells. Ligand engagement dissociates the receptor-coupled heterotrimeric G protein into Gα and Gβγ subunits, initiating distinct downstream cascades that translate the chemokine gradient into directional migration and cytoskeletal reorganization. CXCR5 enables B cells and Tfh cells to follow CXCL13 gradients toward B-cell follicles, establishing the spatial proximity required for productive T cell–B cell interaction, and naive T cells primed by dendritic cells generate CXCR5-positive pre-Tfh cells that migrate along CXCL13 gradients toward follicles, where interactions with cognate B cells license their entry and maturation into fully programmed B-cell helpers. This positioning underlies the generation of high-affinity antibody responses, since Tfh cells are essential contributors to B-cell proliferation, differentiation, and high-affinity antibody synthesis and are required for germinal center formation and maintenance. The axis extends adaptive immune organization into non-lymphoid tissue: CXCL13/CXCR5 activities organize and shape adaptive B-cell-related immune responses outside secondary lymphoid organs through the formation of ectopic lymphoid structures in inflamed tissues, including the central nervous system, and correspondingly, CXCL13 is proposed to recruit B cells to the cerebrospinal fluid during neuroinflammation. In malignancy, receptor engagement reshapes the tumor microenvironment through recruitment of both effector and suppressive populations, so that the CXCL13/CXCR5 axis has a dominant role in B-cell recruitment and tertiary lymphoid structure formation, activating immune responses against some tumors, while in most cancer types the same axis mediates pro-neoplastic immune reactions by recruiting suppressive immune cells into tumor tissue. Disruption of the axis at the developmental level produces measurable structural consequences, as CXCL13/CXCR5-deficient mice show incomplete maturation of lymph nodes. In contrast, overexpression of the pathway causes ectopic lymphoid structures to develop in non-lymphoid tissue.

References
https://pubmed.ncbi.nlm.nih.gov/34947813/ https://pubmed.ncbi.nlm.nih.gov/36078057/

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%