Preferential production of IgG1, IL-4 and IL-10 in MuSK-immunized mice

Ulusoy, Canan; Kim, Eun‐Mi; Tüzün, Erdem; Huda, Ruksana; Yılmaz, Vuslat; Poulas, Konstantinos; Τράκας, Νικόλαος; Skriapa, Lamprini; Niarchos, Athanasios; Strait, Richard T.; Finkelman, Fred D.; Turan, Selin; Zisimopoulou, Paraskevi; Tzartos, Socrates J.; Saruhan‐Direskeneli, Güher; Christadoss, Premkumar

doi:10.1016/j.clim.2014.02.012

Cited by 34 publications

(33 citation statements)

References 23 publications

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“…Another example is in autoimmune glomerulonephropathy wherein mercury exposure results in high serum levels of anti-lamin 1 IgG 1 autoantibody (Kosuda et al, 1998). Preferential production of anti-muscle-specific receptor kinase IgG 1 autoantibody has been observed in a model of Myasthenia gravis in mice (Ulusoy et al, 2014). Intranasal administration of chicken egg ovalbumin was also reported to induce respiratory allergy resulting in augmented serum IgG 1 :IgG 2a ratios (Krieger et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

Aberrant IgG isotype generation in mice with abnormal behaviors

Kim

et al. 2015

Journal of Immunotoxicology

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BTBR T+tf/J (BTBR) mice were recently cited as a suitable animal model for the study of autism because of their behavioral characteristics and immunological changes similar to those reported from autistic subjects. The BTBR mouse was reported to have significantly higher levels of serum IgG, brain IgG deposits and anti-brain IgG than highly social C57BL/6 mice, suggesting involvement of aberrant immune responses in the occurrence of autism. Upregulation of IgG production was investigated here, with a focus on the pattern of IgG isotype distribution compared with that in FVB/NJ (FVB) mice, another highly social control strain. The results indicated that levels of serum IgG 1 , IgG 2b and IgG 3 in post-natal day 21 BTBR mice was significantly higher than FVB mice, regardless of sex, resulting in higher IgG 1 :IgG 2a ratios in BTBR mice than in FVB mice (statistical significance in males). A similar outcome regarding the IgG 1 :IgG 2a ratio was observed in culture supernatants of bone marrow cells from these hosts. A presence of brain-reactive IgG in the sera of BTBR was higher than in FVB mice; levels of brainreactive IgG against whole brain homogenates were higher in BTBR than in FVB mice, with significant differences seen in the striatum and substantia nigra regions. Levels of IgG 1 deposited in the cerebellum, cortex, hippocampus or striatum of both BTBR male and female mice were significantly higher than in FVB counterparts. Overall, these results suggest that alterations in IgG isotype production or deposition in the brain could be implicated in the aberrant immune reactivities of BTBR mice.

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Section: Discussionmentioning

confidence: 99%

Aberrant IgG isotype generation in mice with abnormal behaviors

Kim

et al. 2015

Journal of Immunotoxicology

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“…Most of the C57BL/6, AJ and bm12 mice developed fatiguing weakness after the second or third immunization whereas BALB/c mice produced lower anti-MuSK titers and did not become weak. Some researchers injected more immunogen (20 or 30 μg) and found that the majority of C57BL/ 6 mice developed clinical weakness (Mori et al, 2012b;Ulusoy et al, 2014;Viegas et al, 2012). This was associated with a predominantly IgG1 anti-MuSK response (IgG1 being the nearest mouse analog to human IgG4 with respect to complement activation; Mori et al, 2012b;Ulusoy et al, 2014).…”

Section: Active Immunization Models Of Musk-mgmentioning

confidence: 96%

“…Some researchers injected more immunogen (20 or 30 μg) and found that the majority of C57BL/ 6 mice developed clinical weakness (Mori et al, 2012b;Ulusoy et al, 2014;Viegas et al, 2012). This was associated with a predominantly IgG1 anti-MuSK response (IgG1 being the nearest mouse analog to human IgG4 with respect to complement activation; Mori et al, 2012b;Ulusoy et al, 2014). Complement (C5)-deficient strains (A/ WySnJ, A/J, DBA/2, FVB/N) appeared to be more prone to myasthenic weakness than complement-sufficient strains (B10.A-H2a, BALB/c, and C57BL/6) for reasons that remain unclear (Mori et al, 2012b;Mori and Shigemoto, 2013).…”

Section: Active Immunization Models Of Musk-mgmentioning

confidence: 99%

“…In most studies, the majority of animals developed anti-MuSK antibodies and overt muscle weakness, with evidence of impaired neuromuscular transmission after 2 or 3 immunizations. The immunogen consisted of recombinant extracellular domain of MuSK, from either human (Ulusoy et al, 2014;Viegas et al, 2012), rat (Jha et al, 2006;Mori et al, 2012b;Patel et al, 2014;Punga et al, 2011) or mouse MuSK (Richman et al, 2011;Shigemoto et al, 2006) purified from the conditioned medium of transfected mammalian, insect, yeast or Escherichia coli cells. Richman et al reported consistent weakness in Lewis rats after a single subdermal immunization with 100 μg murine MuSK emulsified in Complete Freunds Adjuvant (CFA), combined with a 2.5 μg subcutaneous (s.c.) injection of pertussis vaccine at a separate site (Richman et al, 2011).…”

Section: Active Immunization Models Of Musk-mgmentioning

confidence: 99%

“…iii) A booster s.c. immunization with the same amount of MuSK emulsified in incomplete Freunds adjuvant (IFA) is given 28 days later. Substitution of IFA for the booster injections did not affect the time-course for weakness development (Ulusoy et al, 2014). iv) Blood samples are taken weekly after the second immunization and anti-MuSK titers are determined by ELISA (Jha et al, 2006).…”

Section: Recommended Protocols For Active Immunization Experiments Inmentioning

confidence: 99%

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