Chapter 7 Studies On The Development of Immunity: The Response To Sheep Red Blood Cells

Auerbach, Robert

doi:10.1016/s0070-2153(08)60074-5

Cited by 12 publications

(6 citation statements)

References 98 publications

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“…Young mice are not totally unresponsive to many antigens. Mice of a variety of strains can produce antibodies against sheep red blood cells injected within the first week of life (Auerbach, 1972). Also, the cell-mediated response causing the regression of tumours induced by murine sarcoma virus in eight strains of mice matures from days 12 to 21 after birth (Gazdar, Beitzel & Talal, 1971).…”

Section: Discussionmentioning

confidence: 99%

Delayed rejection of singleHymenolepis diminutain primary infections of young mice

Befus

Featherston

1974

Parasitology

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In CFLP male tapeworm-free mice, from 2 to 7 weeks old at infection, at least 80% of single Hymenolepis diminuta establish and grow but then are rejected; day of rejection defined as the first day when ≦ 50% of the worms were recovered. Young mice, 2 to 4 weeks old, usually reject their worms during days 16–20 while older mice, 5 to 7 weeks old, reject them during days 12–14. Biomass (total dry weight of all worms recovered on a given day from a group of mice) varied markedly with host age and was consistently greatest in 4-week-old mice. The position of the worm in the intestine did not vary with host age. The quality of mice (categorized by the Medical Research Council Laboratory Animals Centre) did not appear to affect the course of a primary, single H. diminuta infection although, undoubtedly, the mice had varied immunological histories. Variations in time of rejection and biomass of worms recovered are accounted for by both immunological and physiological mechanisms.

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Section: Discussionmentioning

confidence: 99%

Delayed rejection of singleHymenolepis diminutain primary infections of young mice

Befus

Featherston

1974

Parasitology

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“…SRBCs have been widely used as a TD antigen [15][16][17]. To explore the role of Itch deficiency in TD antigens-driven B-cell responses, we used SRBCs to stimulate B-cell activation and antibody production in Itch cKO and their control mice.…”

Section: Itch Deficiency Promoted Antigen-induced B-cell Activation Amentioning

confidence: 99%

The E3 ubiquitin ligase Itch deficiency promotes antigen‐driven B‐cell responses in mice

Fang

Zhai

et al. 2020

Eur J Immunol

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Deficiency of Itch, an E3 ubiquitin ligase, usually induced severe systemic and progressive autoimmune disease. The Itch function is well studied in T cells but not in B cells. We hypothesize that B‐cell‐specific Itch deficiency promoted antigen‐induced B‐cell activation and antibody‐expressing plasma cell (PC) production. We found that unlike Itch KO, Itch cKO (CD19creItchf/f) mice did not demonstrated a significant increase in the sizes of spleens and LNs, antibody level, and base mutation of antibody gene. However, in line with the fact that Itch expression decreased in GC B cells, PCs, and plasmablast (PB)‐like SP 2/0 cells, Itch deficiency promoted B‐cell activation and antibody production induced by antigens including lipopolysaccharide (LPS) and sheep red blood cells (SRBCs). Mechanistically, we found that Itch deficiency promotes antigen‐induced cytokine production because Itch controls the proteins (e.g., eIF3a, eIF3c, eIF3h) with translation initiation factor activity. Altogether, our data suggest that Itch deficiency promotes antigen‐driven B‐cell response. This may provide hints for Itch‐targeted treatment of patients with autoimmune disease.

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“…Studies on the class of antibody evoked after CVB3m challenge of ts 1 survivors are in progress. Neonatal mice are born with functional B lymphocytes (29) and have the capacity for production of specific antibody to many antigens at birth or within a few days after birth (1,7,8,35,46).…”

Section: Infect Immunmentioning

confidence: 99%

“…The ts 1 survivors did not contain detectable levels of anti-CVB3m neutralizing antibody, but upon challenge with CVB3m they produced antibody more rapidly and to higher titers than did normal CD-1 adolescents after primary inoculation with CVB3m. Cell-mediated immunity in ts 1 survivors was compared with that of normal mice after challenge with CVB3m. The capacity for production of migration inhibitory factor was assessed by the agarose droplet cell migration inhibition assay, using peritoneal exudate cells and a CVB3m cell lysate or KClextracted antigens from heart tissues of CVB3m-inoculated mice.…”

mentioning

confidence: 99%

Temperature-Sensitive Mutant of Coxsackievirus B3 Establishes Resistance in Neonatal Mice That Protects Them During Adolescence Against Coxsackievirus B3-Induced Myocarditis

et al. 1983

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Inoculation of neonatal CD-1 mice by multiple routes with an amyocarditic temperature-sensitive (ts) mutant (ts 1) derived from a myocarditic parent variant of coxsackievirus B3 (CVB3m) resulted in approximately half of the neonates surviving to adolescence. Challenge of the ts 1 survivors with CVB3m did not induce myocarditis, as assessed by histological examination of heart tissues. Virus was not detected in heart tissues of adolescent ts 1 survivors, but inoculation of these mice with CVB3m resulted in virus concentrations similar in titers to those found in CVB3m-inoculated normal adolescent mice. The ts 1 survivors did not contain detectable levels of anti-CVB3m neutralizing antibody, but upon challenge with CVB3m they produced antibody more rapidly and to higher titers than did normal CD-1 adolescents after primary inoculation with CVB3m. Cell-mediated immunity in ts 1 survivors was compared with that of normal mice after challenge with CVB3m. The capacity for production of migration inhibitory factor was assessed by the agarose droplet cell migration inhibition assay, using peritoneal exudate cells and a CVB3m cell lysate or KClextracted antigens from heart tissues of CVB3m-inoculated mice. Migration inhibitory factor activity was not detected in cultures of splenic leukocytes from ts 1 survivors of CVB3m-inoculated ts 1 survivors, but it was readily detected in cultures of splenic leukocytes from CVB3m-inoculated normal adolescent mice. The [3H]thymidine stimulation assay, performed with splenic lymphoid cells and purified CVB3m particles, revealed that lymphocytes from normal mice, whether inoculated with CVB3m or not, were not stimulated by CVB3m particle antigens, whereas lymphoid cells from a significantly higher proportion of ts 1 survivors, whether inoculated with CVB3m or not, responded with a stimulation index .2.0. The cells responding with positive stimulation were T lymphocytes. A higher proportion of normal mice and ts 1 survivors, both inoculated with CVB3m, contained splenic cytotoxic T lymphocytes with higher reactivity against CVB3minfected neonatal skin fibroblasts than against normal skin fibroblasts, as assessed by a 51Cr release assay. The group of uninoculated ts 1 survivors present as a high proportion of individuals with cytotoxic T-lymphocyte reactivity against both uninoculated and CVB3m-inoculated skin fibroblasts. However, ts 1 survivors and normal mice possessed the same proportions of splenic lymphocytes carrying either allele for Lyt 1 and Lyt 2 surface markers. The results suggest two mechanisms by which ts 1 survivors exhibit resistance to CVB3m induction of myocarditis, namely, the rapid production of high-titered anti-CVB3m neutralizing antibody in response to CVB3m inoculation and altered cell-mediated immune responses against CVB3m-induced viral or novel cellular antigens. The data are compatible with the notion that an immune deviation mechanism, thought to be controlled through a mechanism requiring suppressor cell activity which inhibits macrophage activation in ts 1...

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Chapter 7 Studies On The Development of Immunity: The Response To Sheep Red Blood Cells

Cited by 12 publications

References 98 publications

Delayed rejection of singleHymenolepis diminutain primary infections of young mice

Delayed rejection of singleHymenolepis diminutain primary infections of young mice

The E3 ubiquitin ligase Itch deficiency promotes antigen‐driven B‐cell responses in mice

Temperature-Sensitive Mutant of Coxsackievirus B3 Establishes Resistance in Neonatal Mice That Protects Them During Adolescence Against Coxsackievirus B3-Induced Myocarditis

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