Changes in suppressor mechanisms during postnatal development in mice.

Calkins, Catherine E.; Stutman, Osias

doi:10.1084/jem.147.1.87

Cited by 50 publications

(16 citation statements)

References 29 publications

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“…Some of the immune deficiencies in immature animals have been ascribed to suppressor mechanisms, though the suppressor activity is reversed before the period where mice remain susceptible to blastomycosis. For example, suppression of contact sensitivity has disappeared by age 5 days (67), suppression of primary and secondary antibody responses has disappeared by age 3 weeks (20,23), non-T-cell suppressors of alloreactivity have disappeared by age 6 days (63), T-cell suppression of mixed lymphocyte cultures has disappeared by 3 weeks (4), and suppression of blastogenesis has disappeared by 4 weeks (37). Suppression of interleukin 2 (IL-2) production lasted until age 6 weeks (5).…”

Section: Discussionmentioning

confidence: 99%

Correlation of Susceptibility of Immature Mice to Fungal Infection (Blastomycosis) and Effector Cell Function

2000

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Immature mice are highly susceptible to blastomycosis, which is similar to other mycoses and has parallels in humans. The murine susceptibility is noteworthy in that it persists beyond the development of resistance to other, nonfungal pathogens and the maturation of most immune functions. As the susceptibility to blastomycosis appeared to be related to an early event after infection, primary effector cell function was studied. We found that peritoneal inflammatory cells, enriched for neutrophils, from immature (3-week-old) mice killed nonphagocytizable Blastomyces dermatitidis cells less (25%) than did cells from mature (8-week) mice (70%) (P < 0.01), a defect intrinsic to the neutrophils. This correlated with an impaired immature cell oxidative burst. Killing of phagocytizable Candida albicans was not significantly different, 73 versus 87%. Thioglycolate-elicited cells were more impaired; killing of B. dermatitidis was insignificant, and killing of C. albicans was more impaired in immature (16% killing) than in mature (45%) cells (P < 0.02). Peripheral blood neutrophils from mature animals killed B. dermatitidis (41%) more than did those from immature animals (10%) (P < 0.02); C. albicans was killed efficiently by both. Resting or activated peritoneal macrophages from both types of animals showed no differences in B. dermatitidis killing. These results suggest that the susceptibility of immature mice is related at least in part to the depressed capacity of their neutrophils to kill B. dermatitidis.Previous studies from our laboratory have shown striking differences in the susceptibilities of immature and mature mice to blastomycosis (8). For example, for challenges via the pulmonary route, 5-week-old mice were 1,000-fold more susceptible than 9-week-old mice. This striking difference in susceptibility was not dependent on the route of challenge. Resistance developed progressively over age 3 to 10 weeks. Studies involving serial sacrifice of infected cohorts revealed that the infectionlimiting event in older mice, i.e., the interval before infectious burdens began to diverge in the two age groups, occurred within 4 days of challenge (8). This timing suggested that the difference in the age groups rested in differences in nonspecific immunity, e.g., activity of effector cells, rather than specific humoral or lymphocyte-mediated immunity, which would require more time for its expression. The studies reported here address the possible mechanism of the age-related differences in immunity, by studying effector cell function.

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Section: Discussionmentioning

confidence: 99%

Correlation of Susceptibility of Immature Mice to Fungal Infection (Blastomycosis) and Effector Cell Function

2000

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“…This possibility was tested in in vitro culture system, using normal bone marrow cells [18][19][20], neonatal spleen cells [21][22][23], and Con A-activated spleen cells [13] as the sources of suppressor cells. As summarized in table III, evidences for the loss of accept ability of suppressive signals in aged spleen cells were not apparent.…”

Section: Discussionmentioning

confidence: 99%

“…This possibility was tested in the following experiments. As the sources of suppressor cells, syngeneic bone marrow cells [18][19][20], neonatal spleen cells [21][22][23], and Con A-activated cells [13] were used. Bone marrow cells were obtained from 3-month-old mice and neonatal spleen cells from 3-to 4-day-old mice.…”

Section: Acceptability Of Splenic Precursors Of Anti-brmrbc Pfc For mentioning

confidence: 99%

Lipopolysaccharide-Induced Autoantibody Response

Fujiwara¹,

Kariyone²

1981

Int Arch Allergy Immunol

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In spleen of normal mice, there are relatively large numbers of plaque-forming cells (PFC) against syngeneic or allogeneic red blood cells treated with bromelain (Br. MRBC) and the numbers of PFC remarkably increase by the injection of bacterial lipopolysacchaiide (LPS). In this report, age-related change in the anti-Br. MRBC PFC response was studied in vivo and in vitro. It was revealed that mean numbers of splenic anti-Br. MRBC PFC increased in both untreated and LPS-injected mice with age (3–14 months). The increase in anti-Br.MRBC PFC detected in LPS-stimulated spleen was dependent on the numbers of PFC in untreated spleen, but not related to the numbers of anti-TNP PFC nor the degree of ³H-thymidine incorporation assessed in in vitro culture. These results imply that enhanced anti-Br.MRBC PFC response was not merely due to polyclonal activation of B lymphocytes. Reasons for increased PFC numbers were analyzed in special references to suppressor activities. The experimental results were obtained suggesting that suppressors were not involved in anti-Br.MRBC PFC response. There were also no marked differences in the acceptability of suppressive signals between young and older spleen cells. It was concluded that hightened anti-Br.MRBC PFC response in older mice might be due to spontaneous increase in the size of Br.MRBC-reactive clone.

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“…Lymphocytes of the thymus were thought to be derived from migrant stem cells from the yolk sac, although recently evidence for an ""embryonic" source has been obtained (20,21 Suppressor cells for antibody reactions are quite abundant in spleens of neonatal mice (26)(27)(28). At least some of these suppressors are Ts cells, since they can be inhibited to some extent by antibodies directed against antigens restricted to T cells.…”

Section: Lymphoid Systemmentioning

confidence: 99%

“…Mice less than three weeks of age not competent for certain humoral and cell-mediated immune reactions (39), and are susceptible to tolerance induction (29). This is due in part to intrinsic susceptibility of B cells to tolerance, frequency or numbers of responsive B cells (40), and an abundance of suppresEnvironmental Health Perspectivessor cells (26)(27)(28).…”

Section: Lymphoid Systemmentioning

confidence: 99%

Effect of Age on Immune Function in Terms of Chemically Induced Cancers

Bennett¹

1979

Environmental Health Perspectives

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Neonatal, fetal, and very old animals are particularly sensitive to chemical carcinogenesis. Reasons for this increased sensitivity could be due to increased susceptibility of "target" organs or cells, peculiar hormonal levels at these age groups, relatively deficient immune functions, or combinations of these and/or other factors. During the late fetal and first three weeks of neonatal life, the immune system is rapidly maturing, is relatively incompetent, and its diverse components are developing at different rates. Gonadotrophic hormones of the pituitary or placenta are high during pregnancy, the early neonatal period, after the menopause, and in a large fraction of men over 60 years of age. These and other hormones are immunosuppressive and could theoretically facilitate carcinogenesis. The particular immune cell type, if any, responsible for resistance to chemically induced tumors has not been determined. One can only state that susceptibility to chemical carcinogenesis is associated with a relative dysfunction of the immune system and that age is an important factor.

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Changes in suppressor mechanisms during postnatal development in mice.

Cited by 50 publications

References 29 publications

Correlation of Susceptibility of Immature Mice to Fungal Infection (Blastomycosis) and Effector Cell Function

Correlation of Susceptibility of Immature Mice to Fungal Infection (Blastomycosis) and Effector Cell Function

Lipopolysaccharide-Induced Autoantibody Response

Effect of Age on Immune Function in Terms of Chemically Induced Cancers

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