GM-CSFR alpha Antibody (698423) [Allophycocyanin]

J774A.1 mouse reticulum cell sarcoma macrophage cell line was stained with Rat Anti-Mouse GM-CSF Ra APC-conjugated Monoclonal Antibody (Catalog # FAB6130A, filled histogram) or isotype control antibody (Catalog # IC006A, open histogram). View our protocol for Staining Membrane-associated Proteins.

GM-CSF-Producing ILCs in Inflamed Joints(A) Flow cytometry analysis of GM-CSF expression by CD4+ T cells and CD4− cells among CD45+ joint infiltrating cells in Rag2−/− mice transferred with CD4+ T cells from WT or Csf2−/− SKG mice.(B) Quantitative RT-PCR analysis of Csf2, Il1b, and Tnf in CD11b+Ly-6G− (CD11b+), CD11b+Ly-6G+ (Ly-6G+), CD4+ T cells, and ILCs sorted from arthritic joints of mannan-treated SKG mice (n = 3). mRNA expression is presented relative to the expression of Hprt1.(C) Flow cytometry of joint infiltrating cells in Rag2−/− mice transferred with CD4+ T cells from WT or Csf2−/− SKG mice. Cells were stained for CD45.2 and lineage markers (a cocktail of CD3, CD4, CD8, CD11b, CD11c, CD19, and DX-5).(D) Proportion of ILCs in Rag2−/− mice transferred with CD4+ T cells as shown in (C). Each symbol represents an individual mouse. Horizontal bars indicate the means.(E) Total cell number of ILCs from healthy or inflamed joints of SKG mice (n = 3).(F) Flow cytometry of synovial ILCs (CD45.2+ lineage markers-negative Thy1.2+ cells as shown in C) for Ki-67 expression.(G) Flow cytometry of synovial ILCs (CD45.2+ lineage markers-negative Thy1.2+ cells as shown in C) for cell surface expression of IL-7Ra, CD25, CCR6, c-kit, IL-33Ra, CD44, and MHC2.(H) Flow cytometry of synovial ILCs (as shown in C) for intranuclear expression of the transcription factor T-bet, Gata-3, Ror gamma t, and Foxp3.(I) Proportion of the transcription factor-expressing synovial ILCs (n = 3) as shown in (H).(J) Flow cytometry of synovial ILCs (as shown in C) for the expression of GM-CSF, Gata-3, and IL-13.(K) Total cell numbers of ILCs from healthy or inflamed joints of C57/BL6 (B6) mice with collagen antibody-induced arthritis (n = 3). Data are representative of two independent experiments.(L) Flow cytometry of synovial ILCs for the expression of GM-CSF and FP635 in arthritic Il17aCre R26RFP635 SKG mice.(M) Quantitative RT-PCR analysis of Csf2 and Bhlhe40 in splenic naive CD25−CD44loCD4+ T cells (naive CD4+ T) and synovial ILCs (n = 3) as shown in (C).(N) The effects of ILC depletion on arthritis development. CD4+ T cells (1 × 106) from Thy1.1+ SKG mice were adoptively transferred into Thy1.2+Rag2−/− mice, which were i.v. injected with 500 μg anti-Thy1.2 mAb or control Rat IgG every week (n = 19 each). The severity of arthritis was monitored every week.∗p < 0.05, ∗∗p < 0.01. Data are representative of three independent experiments in (A)–(C), (E)–(J), (L), and (M) and pooled from more than two experiments in (D), (F), and (N). Vertical bars mean SD in (B), (E), (I), (K), (M), and (N). Image collected and cropped by CiteAb from the following publication (//linkinghub.elsevier.com/retrieve/pii/S1074761318301468), licensed under a CC-BY license. Not internally tested by R&D Systems.

GM-CSF from ILCs and Radio-Resistant Stromal Cells Is Crucial for Autoimmune Arthritis(A) Preparation of experimental groups for assessing arthritogenic effects of GM-CSF from ILCs or radio-resistant stromal cells. Rag2−/− or Csf2−/−Rag2−/− mice were x-irradiated (X-Rag2−/− mice) and transferred with BM cells from Csf2−/− or WT Rag2−/− mice. The resulting four groups of BM chimeras were transferred with CD4+ T cells from Csf2−/− SKG mice 6 weeks after BM reconstitution and assessed for arthritis development 12 weeks later.(B) Arthritis scores of four groups of mice shown in (A).(C) Proportion of total synovial ILCs from x-irradiated Rag2−/− mice reconstituted with Csf2−/− or WT Rag2−/− BM cells.(D) Flow cytometry of synovial ILCs for the expression of GM-CSF and IL-13 in arthritic joints of BM chimeras shown in (C).(E) Proportion of GM-CSF+IL-13−, GM-CSF+IL-13+, and GM-CSF−IL-13+ synovial ILCs (n = 6 each) as shown in (D).(F and G) The effects of ILC depletion on arthritis development. Thy1.1+Rag2−/− mice were x-irradiated and transferred with BM cells from Thy1.1+Rag2−/− and Thy1.2+Csf2−/− SKG mice. The resulting BM chimeras were i.p. injected with 20 mg mannan 6 weeks later, followed by i.v. injection with 500 μg anti-Thy1.1 mAb or control Rat IgG every week. Flow cytometry of synovial ILCs for GM-CSF and IL-13 expression (F). Arthritis scores in each group of mice monitored every week (G). Vertical bars mean SD (n = 8 each).∗p < 0.05, ∗∗p < 0.01. Data are representative of three independent experiments in (D) and (F), and pooled from three experiments in (B), (C), (E), and (G). Horizontal bars indicate the means in (B), (C), and (E). Image collected and cropped by CiteAb from the following publication (//linkinghub.elsevier.com/retrieve/pii/S1074761318301468), licensed under a CC-BY license. Not internally tested by R&D Systems.

GM-CSF-Producing ILCs in Inflamed Joints(A) Flow cytometry analysis of GM-CSF expression by CD4+ T cells and CD4− cells among CD45+ joint infiltrating cells in Rag2−/− mice transferred with CD4+ T cells from WT or Csf2−/− SKG mice.(B) Quantitative RT-PCR analysis of Csf2, Il1b, and Tnf in CD11b+Ly-6G− (CD11b+), CD11b+Ly-6G+ (Ly-6G+), CD4+ T cells, and ILCs sorted from arthritic joints of mannan-treated SKG mice (n = 3). mRNA expression is presented relative to the expression of Hprt1.(C) Flow cytometry of joint infiltrating cells in Rag2−/− mice transferred with CD4+ T cells from WT or Csf2−/− SKG mice. Cells were stained for CD45.2 and lineage markers (a cocktail of CD3, CD4, CD8, CD11b, CD11c, CD19, and DX-5).(D) Proportion of ILCs in Rag2−/− mice transferred with CD4+ T cells as shown in (C). Each symbol represents an individual mouse. Horizontal bars indicate the means.(E) Total cell number of ILCs from healthy or inflamed joints of SKG mice (n = 3).(F) Flow cytometry of synovial ILCs (CD45.2+ lineage markers-negative Thy1.2+ cells as shown in C) for Ki-67 expression.(G) Flow cytometry of synovial ILCs (CD45.2+ lineage markers-negative Thy1.2+ cells as shown in C) for cell surface expression of IL-7Ra, CD25, CCR6, c-kit, IL-33Ra, CD44, and MHC2.(H) Flow cytometry of synovial ILCs (as shown in C) for intranuclear expression of the transcription factor T-bet, Gata-3, Ror gamma t, and Foxp3.(I) Proportion of the transcription factor-expressing synovial ILCs (n = 3) as shown in (H).(J) Flow cytometry of synovial ILCs (as shown in C) for the expression of GM-CSF, Gata-3, and IL-13.(K) Total cell numbers of ILCs from healthy or inflamed joints of C57/BL6 (B6) mice with collagen antibody-induced arthritis (n = 3). Data are representative of two independent experiments.(L) Flow cytometry of synovial ILCs for the expression of GM-CSF and FP635 in arthritic Il17aCre R26RFP635 SKG mice.(M) Quantitative RT-PCR analysis of Csf2 and Bhlhe40 in splenic naive CD25−CD44loCD4+ T cells (naive CD4+ T) and synovial ILCs (n = 3) as shown in (C).(N) The effects of ILC depletion on arthritis development. CD4+ T cells (1 × 106) from Thy1.1+ SKG mice were adoptively transferred into Thy1.2+Rag2−/− mice, which were i.v. injected with 500 μg anti-Thy1.2 mAb or control Rat IgG every week (n = 19 each). The severity of arthritis was monitored every week.∗p < 0.05, ∗∗p < 0.01. Data are representative of three independent experiments in (A)–(C), (E)–(J), (L), and (M) and pooled from more than two experiments in (D), (F), and (N). Vertical bars mean SD in (B), (E), (I), (K), (M), and (N). Image collected and cropped by CiteAb from the following publication (//linkinghub.elsevier.com/retrieve/pii/S1074761318301468), licensed under a CC-BY license. Not internally tested by R&D Systems.

GM-CSF-Producing ILCs in Synovial Fluid of RA Patients(A) The presence of ILCs (defined as CD45+CD3−CD4−CD8−CD11b−CD11c−CD19−CD56−) from peripheral blood (PB) or synovial fluid (SF) of a patient with RA or OA (left). The percentages of ILCs in PB and SF from individual RA (n = 13) or OA (n = 6) patients. The lines indicate the sample pairs of the same patients (right).(B) Total numbers of ILCs in 1 mL of SF from OA and RA patients (n = 6). Vertical bars indicate SD.(C) Flow cytometry analysis of IFN-gamma , IL-13, IL-17, and GM-CSF expression by ILCs (gated as in A) in PB or SF of a RA patient (top). The percentages of cytokine-producing ILCs from individual RA patients (n = 11) (bottom).(D) Gating strategies for GM-CSF+CD45+ lineage markers-negative (ILCs), GM-CSF+CD45+CD3−CD11b+ (myeloid cells), and GM-CSF+CD45+CD11b−CD3+ cells (T cells).(E) Proportion of GM-CSF-producing cells (n = 3). Vertical bars indicate SD. Symbols represent individual samples. Horizontal bars indicate the means.∗p < 0.05, ∗∗p < 0.01. Image collected and cropped by CiteAb from the following publication (//linkinghub.elsevier.com/retrieve/pii/S1074761318301468), licensed under a CC-BY license. Not internally tested by R&D Systems.

GM-CSF from ILCs and Radio-Resistant Stromal Cells Is Crucial for Autoimmune Arthritis(A) Preparation of experimental groups for assessing arthritogenic effects of GM-CSF from ILCs or radio-resistant stromal cells. Rag2−/− or Csf2−/−Rag2−/− mice were x-irradiated (X-Rag2−/− mice) and transferred with BM cells from Csf2−/− or WT Rag2−/− mice. The resulting four groups of BM chimeras were transferred with CD4+ T cells from Csf2−/− SKG mice 6 weeks after BM reconstitution and assessed for arthritis development 12 weeks later.(B) Arthritis scores of four groups of mice shown in (A).(C) Proportion of total synovial ILCs from x-irradiated Rag2−/− mice reconstituted with Csf2−/− or WT Rag2−/− BM cells.(D) Flow cytometry of synovial ILCs for the expression of GM-CSF and IL-13 in arthritic joints of BM chimeras shown in (C).(E) Proportion of GM-CSF+IL-13−, GM-CSF+IL-13+, and GM-CSF−IL-13+ synovial ILCs (n = 6 each) as shown in (D).(F and G) The effects of ILC depletion on arthritis development. Thy1.1+Rag2−/− mice were x-irradiated and transferred with BM cells from Thy1.1+Rag2−/− and Thy1.2+Csf2−/− SKG mice. The resulting BM chimeras were i.p. injected with 20 mg mannan 6 weeks later, followed by i.v. injection with 500 μg anti-Thy1.1 mAb or control Rat IgG every week. Flow cytometry of synovial ILCs for GM-CSF and IL-13 expression (F). Arthritis scores in each group of mice monitored every week (G). Vertical bars mean SD (n = 8 each).∗p < 0.05, ∗∗p < 0.01. Data are representative of three independent experiments in (D) and (F), and pooled from three experiments in (B), (C), (E), and (G). Horizontal bars indicate the means in (B), (C), and (E). Image collected and cropped by CiteAb from the following publication (//linkinghub.elsevier.com/retrieve/pii/S1074761318301468), licensed under a CC-BY license. Not internally tested by R&D Systems.

GM-CSF-Producing ILCs in Inflamed Joints(A) Flow cytometry analysis of GM-CSF expression by CD4+ T cells and CD4− cells among CD45+ joint infiltrating cells in Rag2−/− mice transferred with CD4+ T cells from WT or Csf2−/− SKG mice.(B) Quantitative RT-PCR analysis of Csf2, Il1b, and Tnf in CD11b+Ly-6G− (CD11b+), CD11b+Ly-6G+ (Ly-6G+), CD4+ T cells, and ILCs sorted from arthritic joints of mannan-treated SKG mice (n = 3). mRNA expression is presented relative to the expression of Hprt1.(C) Flow cytometry of joint infiltrating cells in Rag2−/− mice transferred with CD4+ T cells from WT or Csf2−/− SKG mice. Cells were stained for CD45.2 and lineage markers (a cocktail of CD3, CD4, CD8, CD11b, CD11c, CD19, and DX-5).(D) Proportion of ILCs in Rag2−/− mice transferred with CD4+ T cells as shown in (C). Each symbol represents an individual mouse. Horizontal bars indicate the means.(E) Total cell number of ILCs from healthy or inflamed joints of SKG mice (n = 3).(F) Flow cytometry of synovial ILCs (CD45.2+ lineage markers-negative Thy1.2+ cells as shown in C) for Ki-67 expression.(G) Flow cytometry of synovial ILCs (CD45.2+ lineage markers-negative Thy1.2+ cells as shown in C) for cell surface expression of IL-7Ra, CD25, CCR6, c-kit, IL-33Ra, CD44, and MHC2.(H) Flow cytometry of synovial ILCs (as shown in C) for intranuclear expression of the transcription factor T-bet, Gata-3, Ror gamma t, and Foxp3.(I) Proportion of the transcription factor-expressing synovial ILCs (n = 3) as shown in (H).(J) Flow cytometry of synovial ILCs (as shown in C) for the expression of GM-CSF, Gata-3, and IL-13.(K) Total cell numbers of ILCs from healthy or inflamed joints of C57/BL6 (B6) mice with collagen antibody-induced arthritis (n = 3). Data are representative of two independent experiments.(L) Flow cytometry of synovial ILCs for the expression of GM-CSF and FP635 in arthritic Il17aCre R26RFP635 SKG mice.(M) Quantitative RT-PCR analysis of Csf2 and Bhlhe40 in splenic naive CD25−CD44loCD4+ T cells (naive CD4+ T) and synovial ILCs (n = 3) as shown in (C).(N) The effects of ILC depletion on arthritis development. CD4+ T cells (1 × 106) from Thy1.1+ SKG mice were adoptively transferred into Thy1.2+Rag2−/− mice, which were i.v. injected with 500 μg anti-Thy1.2 mAb or control Rat IgG every week (n = 19 each). The severity of arthritis was monitored every week.∗p < 0.05, ∗∗p < 0.01. Data are representative of three independent experiments in (A)–(C), (E)–(J), (L), and (M) and pooled from more than two experiments in (D), (F), and (N). Vertical bars mean SD in (B), (E), (I), (K), (M), and (N). Image collected and cropped by CiteAb from the following publication (//linkinghub.elsevier.com/retrieve/pii/S1074761318301468), licensed under a CC-BY license. Not internally tested by R&D Systems.

GM-CSF-Producing ILCs in Inflamed Joints(A) Flow cytometry analysis of GM-CSF expression by CD4+ T cells and CD4− cells among CD45+ joint infiltrating cells in Rag2−/− mice transferred with CD4+ T cells from WT or Csf2−/− SKG mice.(B) Quantitative RT-PCR analysis of Csf2, Il1b, and Tnf in CD11b+Ly-6G− (CD11b+), CD11b+Ly-6G+ (Ly-6G+), CD4+ T cells, and ILCs sorted from arthritic joints of mannan-treated SKG mice (n = 3). mRNA expression is presented relative to the expression of Hprt1.(C) Flow cytometry of joint infiltrating cells in Rag2−/− mice transferred with CD4+ T cells from WT or Csf2−/− SKG mice. Cells were stained for CD45.2 and lineage markers (a cocktail of CD3, CD4, CD8, CD11b, CD11c, CD19, and DX-5).(D) Proportion of ILCs in Rag2−/− mice transferred with CD4+ T cells as shown in (C). Each symbol represents an individual mouse. Horizontal bars indicate the means.(E) Total cell number of ILCs from healthy or inflamed joints of SKG mice (n = 3).(F) Flow cytometry of synovial ILCs (CD45.2+ lineage markers-negative Thy1.2+ cells as shown in C) for Ki-67 expression.(G) Flow cytometry of synovial ILCs (CD45.2+ lineage markers-negative Thy1.2+ cells as shown in C) for cell surface expression of IL-7Ra, CD25, CCR6, c-kit, IL-33Ra, CD44, and MHC2.(H) Flow cytometry of synovial ILCs (as shown in C) for intranuclear expression of the transcription factor T-bet, Gata-3, Ror gamma t, and Foxp3.(I) Proportion of the transcription factor-expressing synovial ILCs (n = 3) as shown in (H).(J) Flow cytometry of synovial ILCs (as shown in C) for the expression of GM-CSF, Gata-3, and IL-13.(K) Total cell numbers of ILCs from healthy or inflamed joints of C57/BL6 (B6) mice with collagen antibody-induced arthritis (n = 3). Data are representative of two independent experiments.(L) Flow cytometry of synovial ILCs for the expression of GM-CSF and FP635 in arthritic Il17aCre R26RFP635 SKG mice.(M) Quantitative RT-PCR analysis of Csf2 and Bhlhe40 in splenic naive CD25−CD44loCD4+ T cells (naive CD4+ T) and synovial ILCs (n = 3) as shown in (C).(N) The effects of ILC depletion on arthritis development. CD4+ T cells (1 × 106) from Thy1.1+ SKG mice were adoptively transferred into Thy1.2+Rag2−/− mice, which were i.v. injected with 500 μg anti-Thy1.2 mAb or control Rat IgG every week (n = 19 each). The severity of arthritis was monitored every week.∗p < 0.05, ∗∗p < 0.01. Data are representative of three independent experiments in (A)–(C), (E)–(J), (L), and (M) and pooled from more than two experiments in (D), (F), and (N). Vertical bars mean SD in (B), (E), (I), (K), (M), and (N). Image collected and cropped by CiteAb from the following publication (//linkinghub.elsevier.com/retrieve/pii/S1074761318301468), licensed under a CC-BY license. Not internally tested by R&D Systems.

GM-CSF from Non-T Cells Is Crucial for the Initiation of Autoimmune Arthritis(A) Experimental design of adoptive transfer of CD4+ T cells from WT or Csf2−/− SKG mice into Rag2−/− or Csf2−/−Rag2−/− mice. Arthritis scores of four groups (a–d) of mice were assessed 3 months after transfer of 1 × 106 CD4+ T cells.(B) Arthritis scores of the four groups mice (n = 15 or 16 each) shown in (A). Horizontal bars indicate the means.(C) Representative joint histology of the groups shown in (A). Scale bars indicate 200 μm.(D) Flow cytometry of splenic CD4+ T cells stained for intracellular IL-17 and GM-CSF or IFN-gamma .(E) Proportion of IL-17-producing CD4+ T cells from individual mice as shown in (D). Vertical bars mean SD (n = 3).∗∗p < 0.01. Data are representative of three independent experiments (C–E) or pooled from three independent experiments (B). Image collected and cropped by CiteAb from the following publication (//linkinghub.elsevier.com/retrieve/pii/S1074761318301468), licensed under a CC-BY license. Not internally tested by R&D Systems.

GM-CSF-Producing ILCs in Synovial Fluid of RA Patients(A) The presence of ILCs (defined as CD45+CD3−CD4−CD8−CD11b−CD11c−CD19−CD56−) from peripheral blood (PB) or synovial fluid (SF) of a patient with RA or OA (left). The percentages of ILCs in PB and SF from individual RA (n = 13) or OA (n = 6) patients. The lines indicate the sample pairs of the same patients (right).(B) Total numbers of ILCs in 1 mL of SF from OA and RA patients (n = 6). Vertical bars indicate SD.(C) Flow cytometry analysis of IFN-gamma , IL-13, IL-17, and GM-CSF expression by ILCs (gated as in A) in PB or SF of a RA patient (top). The percentages of cytokine-producing ILCs from individual RA patients (n = 11) (bottom).(D) Gating strategies for GM-CSF+CD45+ lineage markers-negative (ILCs), GM-CSF+CD45+CD3−CD11b+ (myeloid cells), and GM-CSF+CD45+CD11b−CD3+ cells (T cells).(E) Proportion of GM-CSF-producing cells (n = 3). Vertical bars indicate SD. Symbols represent individual samples. Horizontal bars indicate the means.∗p < 0.05, ∗∗p < 0.01. Image collected and cropped by CiteAb from the following publication (//linkinghub.elsevier.com/retrieve/pii/S1074761318301468), licensed under a CC-BY license. Not internally tested by R&D Systems.

GM-CSF-Producing ILCs in Inflamed Joints(A) Flow cytometry analysis of GM-CSF expression by CD4+ T cells and CD4− cells among CD45+ joint infiltrating cells in Rag2−/− mice transferred with CD4+ T cells from WT or Csf2−/− SKG mice.(B) Quantitative RT-PCR analysis of Csf2, Il1b, and Tnf in CD11b+Ly-6G− (CD11b+), CD11b+Ly-6G+ (Ly-6G+), CD4+ T cells, and ILCs sorted from arthritic joints of mannan-treated SKG mice (n = 3). mRNA expression is presented relative to the expression of Hprt1.(C) Flow cytometry of joint infiltrating cells in Rag2−/− mice transferred with CD4+ T cells from WT or Csf2−/− SKG mice. Cells were stained for CD45.2 and lineage markers (a cocktail of CD3, CD4, CD8, CD11b, CD11c, CD19, and DX-5).(D) Proportion of ILCs in Rag2−/− mice transferred with CD4+ T cells as shown in (C). Each symbol represents an individual mouse. Horizontal bars indicate the means.(E) Total cell number of ILCs from healthy or inflamed joints of SKG mice (n = 3).(F) Flow cytometry of synovial ILCs (CD45.2+ lineage markers-negative Thy1.2+ cells as shown in C) for Ki-67 expression.(G) Flow cytometry of synovial ILCs (CD45.2+ lineage markers-negative Thy1.2+ cells as shown in C) for cell surface expression of IL-7Ra, CD25, CCR6, c-kit, IL-33Ra, CD44, and MHC2.(H) Flow cytometry of synovial ILCs (as shown in C) for intranuclear expression of the transcription factor T-bet, Gata-3, Ror gamma t, and Foxp3.(I) Proportion of the transcription factor-expressing synovial ILCs (n = 3) as shown in (H).(J) Flow cytometry of synovial ILCs (as shown in C) for the expression of GM-CSF, Gata-3, and IL-13.(K) Total cell numbers of ILCs from healthy or inflamed joints of C57/BL6 (B6) mice with collagen antibody-induced arthritis (n = 3). Data are representative of two independent experiments.(L) Flow cytometry of synovial ILCs for the expression of GM-CSF and FP635 in arthritic Il17aCre R26RFP635 SKG mice.(M) Quantitative RT-PCR analysis of Csf2 and Bhlhe40 in splenic naive CD25−CD44loCD4+ T cells (naive CD4+ T) and synovial ILCs (n = 3) as shown in (C).(N) The effects of ILC depletion on arthritis development. CD4+ T cells (1 × 106) from Thy1.1+ SKG mice were adoptively transferred into Thy1.2+Rag2−/− mice, which were i.v. injected with 500 μg anti-Thy1.2 mAb or control Rat IgG every week (n = 19 each). The severity of arthritis was monitored every week.∗p < 0.05, ∗∗p < 0.01. Data are representative of three independent experiments in (A)–(C), (E)–(J), (L), and (M) and pooled from more than two experiments in (D), (F), and (N). Vertical bars mean SD in (B), (E), (I), (K), (M), and (N). Image collected and cropped by CiteAb from the following publication (//linkinghub.elsevier.com/retrieve/pii/S1074761318301468), licensed under a CC-BY license. Not internally tested by R&D Systems.

• Reactivity: Mu
• Applications: Flow
• Clone: 698423
• Clonality: Monoclonal
• Host: Rat
• Conjugate: Allophycocyanin

GM-CSFR alpha Antibody (698423) [Allophycocyanin] Summary

• Immunogen: Mouse myeloma cell line NS0-derived recombinant mouse GM-CSF R alpha
  Leu30-Pro327
  Accession # Q00941
• Specificity: Detects mouse GM-CSF R alpha in direct ELISAs. In direct ELISAs, no cross-reactivity with recombinant human (rh) GM-CSF R alpha or rhGM‑CSF R beta is observed.
• Source: N/A
• Isotype: IgG2a
• Clonality: Monoclonal
• Host: Rat
• Gene: CSF2RA
• Purity Statement: Protein A or G purified from hybridoma culture supernatant

Applications/Dilutions

• Dilutions:
  • Flow Cytometry 10 uL/10^6 cells

Packaging, Storage & Formulations

• Storage: Protect from light. Do not freeze.
  • 12 months from date of receipt, 2 to 8 °C as supplied.
• Buffer: Supplied in a saline solution containing BSA and Sodium Azide.
• Preservative: Sodium Azide

Notes

This product is produced by and ships from R&D Systems, Inc., a Bio-Techne brand.

Alternate Names for GM-CSFR alpha Antibody (698423) [Allophycocyanin]

• CD116 antigen
• CD116
• CDw116
• colony stimulating factor 2 receptor alpha subunit
• colony stimulating factor 2 receptor, alpha, low-affinity(granulocyte-macrophage)
• CSF2R
• CSF2RA
• CSF2RAX
• CSF2RAY
• CSF2RX
• CSF2RY
• GM-CSF R alpha
• GM-CSF receptor alpha subunit
• GMCSFR alpha
• GMCSFR
• GM-CSFRa
• GM-CSF-R-alpha
• GMCSFR-alpha
• GMR
• GMR-alpha
• granulocyte-macrophage colony-stimulating factor receptor alpha chain
• granulocyte-macrophage colony-stimulating factor receptor subunit alpha
• MGC3848
• MGC4838

Background

Granulocyte macrophage colony stimulating factor receptor alpha (GM-CSF R alpha ), also known as CD116, is a component of the receptor complex that mediates cellular responses to GM-CSF. GM-CSF promotes the differentiation and mobilization of granulocyte-macrophage, erythroid, megakaryocyte, and eosinophil progenitors. It enhances the activation of myeloid cell effector functions and plays a role in the development of Th1 biased immune responses, allergic inflammation, and autoimmunity (1-4). Mature mouse GM-CSF R alpha is an 80 kDa type I transmembrane glycoprotein that consists of a 298 amino acid (aa) extracellular domain (ECD) with two fibronectin type III domains and a juxtamembrane WSXWS motif, a 21 aa transmembrane segment, and a 40 aa cytoplasmic domain (5). Within the ECD, mouse GM-CSF R alpha shares approximately 33% and 58% aa sequence identity with human and rat GM-CSF R alpha , respectively. Soluble forms of the human receptor retain the ability to bind GM-CSF (6, 7). GM-CSF R alpha is expressed on hematopoietic stem cells, progenitor and differentiated cells in the myeloid lineage, vascular endothelial cells, placenta, and non‑hematopoietic solid tumor cells (8). GM-CSF R alpha associates with the common beta chain/CD131 ( beta _c), a 135 kDa transmembrane protein that is also the signal transducing component of the receptors for IL-3 and IL-5 (9, 10). Association with beta _c converts GM-CSF R alpha from a low affinity to a high affinity receptor for GM-CSF (9-11). The shared usage of beta _c underlies the synergism between GM-CSF, IL-3, and IL-5 in their effects on myeloid cell differentiation and activation (1, 2).

1. Martinez-Moczygemba, M. and D.P. Huston (2003) J. Allergy Clin. Immunol. 112:653.
2. Fleetwood, A.J. et al. (2005) Crit. Rev. Immunol. 25:405.
3. Eksioglu, E.A. et al. (2007) Exp. Hematol. 35:1163.
4. Cao, Y. (2007) J. Clin. Invest. 117:2362.
5. Park, L.S. et al. (1992) Proc. Natl. Acad. Sci. 89:4295.
6. Pelley, J.L. et al. (2007) Exp. Hematol. 35:1483.
7. Raines, M.A. et al. (1991) Proc. Natl. Acad. Sci. 88:8203.
8. Chiba, S. et al. (1990) Cell Regul. 1:327.
9. Kitamura, T. et al. (1991) Proc. Natl. Acad. Sci. 88:5082.
10. Hayashida, K. et al. (1990) Proc. Natl. Acad. Sci. 87:9655.
11. Hoang, T. et al. (1993) J. Biol. Chem. 268:11881.

Limitations

This product is for research use only and is not approved for use in humans or in clinical diagnosis. Primary Antibodies are guaranteed for 1 year from date of receipt.

Publications for GM-CSFR alpha Antibody (FAB6130A)(6)

Publications using FAB6130A

• T Fukaya, T Uto, S Mitoma, H Takagi, Y Nishikawa, M Tominaga, N Choijookhu, Y Hishikawa, K Sato Gut dysbiosis promotes the breakdown of oral tolerance mediated through dysfunction of mucosal dendritic cells Cell Reports, 2023-04-25;42(5):112431. 2023-04-25 [PMID: 37099426]
• K Ogawa, M Tsurutani, A Hashimoto, M Soeda Simple propagation method for resident macrophages by co-culture and subculture, and their isolation from various organs BMC Immunol., 2019-09-18;20(1):34. 2019-09-18 [PMID: 31533615] (Flow Cytometry, Mouse)
• Keiji Hirota, Motomu Hashimoto, Yoshinaga Ito, Mayumi Matsuura, Hiromu Ito, Masao Tanaka et al. Autoimmune Th17 Cells Induced Synovial Stromal and Innate Lymphoid Cell Secretion of the Cytokine GM-CSF to Initiate and Augment Autoimmune Arthritis Immunity 2018-06-19 [PMID: 29802020]
• K Miyake, N Shiozawa, T Nagao, S Yoshikawa, Y Yamanishi, H Karasuyama Trogocytosis of peptide-MHC class II complexes from dendritic cells confers antigen-presenting ability on basophils Proc. Natl. Acad. Sci. U.S.A, 2017-01-17;0(0):. 2017-01-17 [PMID: 28096423] (Flow Cytometry, Mouse)
• Zhou Q, Ho A, Schlitzer A, Tang Y, Wong K, Wong F, Chua Y, Angeli V, Mortellaro A, Ginhoux F, Kemeny D GM-CSF-licensed CD11b+ lung dendritic cells orchestrate Th2 immunity to Blomia tropicalis. J Immunol, 2014-06-18;193(2):496-509. 2014-06-18 [PMID: 24943219] (Flow Cytometry, Mouse)
• van Nieuwenhuijze A, Coghill E, Gray D, Prato S, Metcalf D, Alexander W, Wicks I Transgenic expression of GM-CSF in T cells causes disseminated histiocytosis. Am J Pathol, 2013-10-30;184(1):184-99. 2013-10-30 [PMID: 24183847] (Flow Cytometry, Mouse)

Bioinformatics

• Gene Symbol: CSF2RA
• Uniprot:
  • Q00941()