CXCL13 Antibody (Rabbit mAb) [N2C21]

Application: Reactivity: Human

Usage Information

Dilution
IHC1:1000

Application
IHC

Reactivity
Human

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	Human colon tissue; Human kidney tissue; Human tonsil tissue
Negative Control

Datasheet & SDS

Biological Description

Specificity
CXCL13 Antibody (Rabbit mAb) [N2C21] detects endogenous levels of total CXCL13 protein.

Clone
N2C21

Synonym(s)
BCA1, BLC, SCYB13, CXCL13, C-X-C motif chemokine 13, Angie, B cell-attracting chemokine 1, B lymphocyte chemoattractant, CXC chemokine BLC, Small-inducible cytokine B13, BCA-1

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. Follicular dendritic cells, stromal cells, and marginal reticular cells within secondary lymphoid organs constitutively secrete CXCL13, establishing chemotactic gradients that direct naive B cells and CXCR5-expressing T follicular helper (Tfh) cells toward B-cell follicles. Receptor engagement triggers heterotrimeric G-protein-coupled signaling that activates the Rac GTPase pathway through the guanine exchange factor DOCK2 together with phosphoinositide-3 kinase δ, driving F-actin polymerization and directional cell migration; these two pathways act in a complementary manner, since disruption of either alone only partially compromises follicular entry while combined loss abolishes it. Within the follicle, CXCR5 cooperates with the integrin LFA-1 and its ligand ICAM-1 to sustain B-cell surveillance of the follicular dendritic cell network, and B-cell receptor engagement subsequently reshapes this migratory behavior by segregating CXCR5 to the periphery of the immunological synapse, coupling antigen recognition with continued positional control. This spatial choreography positions B cells for productive interaction with Tfh cells, which supports germinal center formation, immunoglobulin affinity maturation, and long-term humoral memory. Physiological relevance extends to a positive feedback loop between B cells and follicular dendritic cells that reinforces follicle development and sustains secondary lymphoid organ homeostasis. Elevated CXCL13/CXCR5 signaling contributes to tertiary lymphoid structure formation and, depending on tumor context, mediates either protective anti-tumor immune activation or recruitment of immunosuppressive populations into the tumor microenvironment, while chronic axis engagement in autoimmune and neuroinflammatory settings drives ectopic B-cell recruitment, including migration into the cerebrospinal fluid during central nervous system inflammation.

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. Follicular dendritic cells, stromal cells, and marginal reticular cells within secondary lymphoid organs constitutively secrete CXCL13, establishing chemotactic gradients that direct naive B cells and CXCR5-expressing T follicular helper (Tfh) cells toward B-cell follicles. Receptor engagement triggers heterotrimeric G-protein-coupled signaling that activates the Rac GTPase pathway through the guanine exchange factor DOCK2 together with phosphoinositide-3 kinase δ, driving F-actin polymerization and directional cell migration; these two pathways act in a complementary manner, since disruption of either alone only partially compromises follicular entry while combined loss abolishes it. Within the follicle, CXCR5 cooperates with the integrin LFA-1 and its ligand ICAM-1 to sustain B-cell surveillance of the follicular dendritic cell network, and B-cell receptor engagement subsequently reshapes this migratory behavior by segregating CXCR5 to the periphery of the immunological synapse, coupling antigen recognition with continued positional control. This spatial choreography positions B cells for productive interaction with Tfh cells, which supports germinal center formation, immunoglobulin affinity maturation, and long-term humoral memory. Physiological relevance extends to a positive feedback loop between B cells and follicular dendritic cells that reinforces follicle development and sustains secondary lymphoid organ homeostasis. Elevated CXCL13/CXCR5 signaling contributes to tertiary lymphoid structure formation and, depending on tumor context, mediates either protective anti-tumor immune activation or recruitment of immunosuppressive populations into the tumor microenvironment, while chronic axis engagement in autoimmune and neuroinflammatory settings drives ectopic B-cell recruitment, including migration into the cerebrospinal fluid during central nervous system inflammation.

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

Reference Table for Selecting PVDF Membrane Pore Size Specifications

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%