Phenotypes associated with this allele

• Allele Symbol: Cd69^tm1Naka
• Allele Name: targeted mutation 1, Toshinori Nakayama
• Allele ID: MGI:2675144
• Summary: 2 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Cd69^tm1Naka/Cd69^tm1Naka	B6.129P2-Cd69^tm1Naka	MGI:5426964
hm2	Cd69^tm1Naka/Cd69^tm1Naka	C.129P2-Cd69^tm1Naka	MGI:2675163

Genotype
MGI:5426964

hm1

• Allelic Composition: Cd69^tm1Naka/Cd69^tm1Naka
• Genetic Background: B6.129P2-Cd69^tm1Naka

• ♀: phenotype observed in females
• ♂: phenotype observed in males
• N: normal phenotype

immune system

decreased CD4-positive, alpha-beta T cell number ( J:184704 )

• fewer CD44^hi CD154+ CD4+ T cells in the bone marrow

abnormal T cell physiology ( J:184704 )

• honing of effector and memory T helper cells to the bone marrow is impaired compared to in wild-type cells

• persistence of T helper cells on bone marrow stromal cells is impaired compared to in wild-type mice

abnormal CD4-positive, alpha-beta T cell physiology ( J:184704 )

• CD4+ T cells fail to induce production of high-affinity antibodies, especially in the late phase, compared with wild-type cells

abnormal memory T cell physiology ( J:184704 )

• bone marrow memory T cells induce less efficiently the production of high-affinity antibodies compared with wild-type cells

abnormal humoral immune response ( J:184704 )

• mice immunized with NP-CGG plus LPS or NP-KLH produce less NP-specific high-affinity antibodies compared with wild-type mice

• however, T follicular helper cells and germinal center B cells are normally generated

decreased interferon-gamma secretion ( J:184704 )

• from CD4+ T cells stimulated with anti-CD3 antibodies in the presence of brefeldin A

decreased tumor necrosis factor secretion ( J:184704 )

• from CD4+ T cells stimulated with anti-CD3 antibodies in the presence of brefeldin A

hematopoietic system

decreased CD4-positive, alpha-beta T cell number ( J:184704 )

• fewer CD44^hi CD154+ CD4+ T cells in the bone marrow

abnormal T cell physiology ( J:184704 )

• honing of effector and memory T helper cells to the bone marrow is impaired compared to in wild-type cells

• persistence of T helper cells on bone marrow stromal cells is impaired compared to in wild-type mice

abnormal CD4-positive, alpha-beta T cell physiology ( J:184704 )

• CD4+ T cells fail to induce production of high-affinity antibodies, especially in the late phase, compared with wild-type cells

abnormal memory T cell physiology ( J:184704 )

• bone marrow memory T cells induce less efficiently the production of high-affinity antibodies compared with wild-type cells

Genotype
MGI:2675163

hm2

• Allelic Composition: Cd69^tm1Naka/Cd69^tm1Naka
• Genetic Background: C.129P2-Cd69^tm1Naka

immune system

impaired neutrophil chemotaxis ( J:84940 )

• RT-PCR analysis revealed significantly decreased CXCL1 expression levels in mutant hind paws at 4 days after treatment with anti-type II collagen antibodies and LPS, suggesting that neutrophil migration in mutant arthritic joints is reduced

• on day 10 after treatment, MCP-1 and MCP-2 expression levels in mutant mice are significantly lower than those of wild-type mice

impaired neutrophil recruitment ( J:84940 )

• at 10 days after anti-type II collagen antibody injection, neutrophil infiltration in mutant arthritic joints is reduced relative to that in similarly-treated wild-type joints

decreased susceptibility to induced arthritis ( J:84940 )

• homozygotes exhibit a less severe arthritic response to anti-type II collagen antibodies relative to similarly-treated wild-type mice

• unlike in wild-type mice, no rigidity or massive swelling is observed in mutant joints at 10 days after treatment with anti-type II collagen antibodies and LPS

• at 10 days after anti-type II collagen antibody injection, neutrophil infiltration is dramatically reduced in mutant joints relative to that in similarly-treated wild-type joints

• RT-PCR analysis revealed that mRNA levels of IL-1beta, IL-6 and MCP-1 are significantly reduced in mutant arthritic joints at 4 and 10 days after antibody injection relative to those in similarly-treated wild-type mice

• cell transfer of wild-type neutrophils, but not T cells or spleen cells, can restore the anti-type II collagen-mediated arthritic response in mutant mice to almost normal levels

skeleton

decreased susceptibility to induced arthritis ( J:84940 )

• homozygotes exhibit a less severe arthritic response to anti-type II collagen antibodies relative to similarly-treated wild-type mice

• unlike in wild-type mice, no rigidity or massive swelling is observed in mutant joints at 10 days after treatment with anti-type II collagen antibodies and LPS

• at 10 days after anti-type II collagen antibody injection, neutrophil infiltration is dramatically reduced in mutant joints relative to that in similarly-treated wild-type joints

• RT-PCR analysis revealed that mRNA levels of IL-1beta, IL-6 and MCP-1 are significantly reduced in mutant arthritic joints at 4 and 10 days after antibody injection relative to those in similarly-treated wild-type mice

• cell transfer of wild-type neutrophils, but not T cells or spleen cells, can restore the anti-type II collagen-mediated arthritic response in mutant mice to almost normal levels

cellular

impaired neutrophil chemotaxis ( J:84940 )

• RT-PCR analysis revealed significantly decreased CXCL1 expression levels in mutant hind paws at 4 days after treatment with anti-type II collagen antibodies and LPS, suggesting that neutrophil migration in mutant arthritic joints is reduced

• on day 10 after treatment, MCP-1 and MCP-2 expression levels in mutant mice are significantly lower than those of wild-type mice

hematopoietic system

impaired neutrophil chemotaxis ( J:84940 )

• RT-PCR analysis revealed significantly decreased CXCL1 expression levels in mutant hind paws at 4 days after treatment with anti-type II collagen antibodies and LPS, suggesting that neutrophil migration in mutant arthritic joints is reduced

• on day 10 after treatment, MCP-1 and MCP-2 expression levels in mutant mice are significantly lower than those of wild-type mice

impaired neutrophil recruitment ( J:84940 )

• at 10 days after anti-type II collagen antibody injection, neutrophil infiltration in mutant arthritic joints is reduced relative to that in similarly-treated wild-type joints