Phenotypes associated with this allele

• Allele Symbol: Tg(LCK-NFKBIA)5Dwb
• Allele Name: transgene insertion 5, Dean W Ballard
• Allele ID: MGI:3056807
• Summary: 3 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
cx1	Tg(LCK-NFKBIA)5Dwb/? Tg(Tcra,Tcrb)1Mcd/?	involves: BALB/c * C57BL/6 * DBA/2	MGI:3835055
tg2	Tg(LCK-NFKBIA)5Dwb/0	involves: C57BL/6 * DBA/2	MGI:3834909
tg3	Tg(LCK-NFKBIA)5Dwb/?	involves: BALB/c * C57BL/6 * DBA/2	MGI:3835054

Genotype
MGI:3835055

cx1

• Allelic Composition: Tg(LCK-NFKBIA)5Dwb/?; Tg(Tcra,Tcrb)1Mcd/?
• Genetic Background: involves: BALB/c * C57BL/6 * DBA/2

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

immune system

decreased interferon-gamma secretion ( J:145531 )

• mutant T cells produce very little IFN-gamma when transferred into host that is immunized with hemagglutinin

Genotype
MGI:3834909

tg2

• Allelic Composition: Tg(LCK-NFKBIA)5Dwb/0
• Genetic Background: involves: C57BL/6 * DBA/2

immune system

increased T cell apoptosis ( J:93003 )

• about twice the percentage of T cells are apoptotic after in vitro stimulation with Con-A

• this is observed for both CD4⁺ and CD8⁺ T cells

• anti-TCR stimulation produces similar results with more enhanced apoptosis observed for CD8⁺ T cells

decreased T cell proliferation ( J:93003 )

• thymocyotes only have one third the proliferation rate as controls when stimulated with PMA and ionomycin

• thymocyte proliferation is also severely curtailed in response to other mitogens

• addition of IL-2 to culture does not rescue the proliferation defect

• similar results were observed for B cell-depleted splenocytes

abnormal CD8-positive, alpha-beta T cell differentiation ( J:93003 )

• numbers of CD8 single-positive thymocytes bearing high levels of TCR are reduced by 40% compared to controls

decreased CD4-positive, alpha-beta T cell number ( J:93003 )

• CD4⁺ T cell numbers are reduced in the spleen, lymph nodes, and blood though not to the degree of reduction observed for CD8⁺ T cells

decreased CD8-positive, alpha-beta T cell number ( J:93003 )

• CD8⁺ T cell numbers are reduced by two-thirds or more in the spleen, lymph nodes, and blood

decreased interleukin-2 secretion ( J:93003 )

• thymocytes produce about 20-fold less IL-2 when stimulated compared to wild-type controls

• likewise, splenocytes only produce 8% the IL-2 as controls when stimulated

hematopoietic system

increased T cell apoptosis ( J:93003 )

• about twice the percentage of T cells are apoptotic after in vitro stimulation with Con-A

• this is observed for both CD4⁺ and CD8⁺ T cells

• anti-TCR stimulation produces similar results with more enhanced apoptosis observed for CD8⁺ T cells

decreased T cell proliferation ( J:93003 )

• thymocyotes only have one third the proliferation rate as controls when stimulated with PMA and ionomycin

• thymocyte proliferation is also severely curtailed in response to other mitogens

• addition of IL-2 to culture does not rescue the proliferation defect

• similar results were observed for B cell-depleted splenocytes

abnormal CD8-positive, alpha-beta T cell differentiation ( J:93003 )

• numbers of CD8 single-positive thymocytes bearing high levels of TCR are reduced by 40% compared to controls

decreased CD4-positive, alpha-beta T cell number ( J:93003 )

• CD4⁺ T cell numbers are reduced in the spleen, lymph nodes, and blood though not to the degree of reduction observed for CD8⁺ T cells

decreased CD8-positive, alpha-beta T cell number ( J:93003 )

• CD8⁺ T cell numbers are reduced by two-thirds or more in the spleen, lymph nodes, and blood

cellular

increased T cell apoptosis ( J:93003 )

• about twice the percentage of T cells are apoptotic after in vitro stimulation with Con-A

• this is observed for both CD4⁺ and CD8⁺ T cells

• anti-TCR stimulation produces similar results with more enhanced apoptosis observed for CD8⁺ T cells

decreased T cell proliferation ( J:93003 )

• thymocyotes only have one third the proliferation rate as controls when stimulated with PMA and ionomycin

• thymocyte proliferation is also severely curtailed in response to other mitogens

• addition of IL-2 to culture does not rescue the proliferation defect

• similar results were observed for B cell-depleted splenocytes

Genotype
MGI:3835054

tg3

• Allelic Composition: Tg(LCK-NFKBIA)5Dwb/?
• Genetic Background: involves: BALB/c * C57BL/6 * DBA/2

immune system

abnormal T-helper 1 physiology ( J:145531 )

• the decreased delayed type hypersensitivity response to antigen rechallenge and the decreased IFN-gamma secretion by T cells isolated from the draining lymph nodes to these rechallenged areas demonstrate a defective Th1 response

• defective class switching of antigen-specific immunoglobulin to IgG2a gives further evidence of a defective Th1-response

decreased susceptibility to type I hypersensitivity reaction ( J:145531 )

• antigen rechallenge in the lung leads to slightly less periarterial inflammation than in controls

• there is significant attenuation of airway hyperresponsiveness in these mice upon antigen rechallenge in the lung

• the number of cells isolated from BAL fluid in these aerosol rechallenged mice is one-third of controls

• the level of antigen-specific IgG2a in aerosol sensitized mice is markedly reduced

decreased susceptibility to type IV hypersensitivity reaction ( J:145531 )

• antigenic challenge after prior sensitization leads to 4-fold less swelling in the footpads compared to controls

decreased interferon-gamma secretion ( J:145531 )

• T cells isolated from the draining lymph nodes of mice rechallenged with antigen produce significantly less IFN-gamma than controls

hematopoietic system

abnormal T-helper 1 physiology ( J:145531 )

• the decreased delayed type hypersensitivity response to antigen rechallenge and the decreased IFN-gamma secretion by T cells isolated from the draining lymph nodes to these rechallenged areas demonstrate a defective Th1 response

• defective class switching of antigen-specific immunoglobulin to IgG2a gives further evidence of a defective Th1-response