Lymphocyte Proliferative Responsiveness in 31 Patients after an Outbreak of Toxoplasmosis

Se, Maddison; Sb, Slemenda; Sm, Teutsch; Kw, Walls; Ig, Kagan; Wr, Mason; Bell, Fiona; Smith, James R.

doi:10.4269/ajtmh.1979.28.955

Cited by 13 publications

(4 citation statements)

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“…Lymphocyte proliferation to T. gondii antigens has been shown to be a specific indicator of prior T. gondii infection in adults [233,234,567,568]. This technique has been found useful in establishing the diagnosis of congenital T. gondii infection in some infants [480,569,570].…”

Section: Tests Of Cell-mediated Immunitymentioning

confidence: 99%

Toxoplasmosis

Remington¹,

McLeod²,

Wilson³

et al. 2011

Infectious Diseases of the Fetus and Newborn

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Section: Tests Of Cell-mediated Immunitymentioning

confidence: 99%

Toxoplasmosis

Remington¹,

McLeod²,

Wilson³

et al. 2011

Infectious Diseases of the Fetus and Newborn

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“…Nonetheless, there is substantial evidence to suggest that environmental transmission of Toxoplasma is significant. The oocyst stage is linked to large outbreaks of toxoplasmosis (Bowie et al ., 1997; Maddison et al ., 1979; Teutsch et al ., 1979; Stagno et al ., 1980; Benenson et al ., 1982; Bahia‐Oliveira et al ., 2003) whereas epidemics caused by food contamination are typically smaller and less frequently reported (Kean et al ., 1969; Fertig et al ., 1977; Robson et al ., 1995). A number of studies have convincingly related environmental factors to toxoplasmosis risk (Tenter et al ., 2000) including a recent large multicentre study in Europe linking soil contact to T. gondii infection (Cook et al ., 2000), and studies of suburban populations of Campos dos Goytacazes, Brazil, that demonstrate high T. gondii infection rates are primarily caused by exposure to tainted water (Bahia‐Oliveira et al ., 2003).…”

Section: Introductionmentioning

confidence: 99%

Identification of a sporozoite‐specific member of the Toxoplasma SAG superfamily via genetic complementation

Radke

Gubbels

Jerome

et al. 2004

Molecular Microbiology

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SummaryToxoplasma gondii sporozoites possess an array of stage-specific antigens that are localized to the membrane and internal cellular space, as well as secreted into the primary parasitophorous vacuole. Specific labelling of viable sporozoites excysted from oocysts reveals a complex admixture of surface proteins partially shared with tachyzoites. SAG1, SRS3 and SAG3 were detected on sporozoites as well as numerous minor antigens. In contrast, tachyzoite SAG2A and B were completely absent whereas a dominant 25 kDa protein was unique to the sporozoite surface. The sporozoite gene encoding this protein was identified in tachyzoites genetically complemented with a sporozoite cDNA library and cloned via site-specific recombination into a bacterial shuttle vector. The sporozoite cDNA identified in these experiments encoded a protein with conserved structural features of the prototypical T. gondii SAG1 (P30) and shared sequence identity with surface proteins from Sarcocystis spp. This new member of the SAG superfamily was designated SporoSAG. Expression of SporoSAG in tachyzoites conferred enhanced invasion on transgenic parasites suggesting a role for this protein in oocyst/sporozoite transmission to susceptible hosts.

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“…Toxoplasma infection in mice and in humans has been associated with transient immune dysfunction manifest as reduced delayed hypersensitivity (DTH) responses (Jones 1980, Krahenbuhl & Remington 1982, varying degrees of in vitro proliferative responses to toxoplasma antigen in the first months after the illness (Anderson et al 1981 Krahenbuhl et al 1971, Maddison et at. 1979 and, in some patients and animal models, delayed appearance of lymphokines which activate mononuclear cells to inhibit toxoplasma (Johnson 198 1, Jones et al 1977).…”

Section: Introductionmentioning

confidence: 99%

Murine spleen and lymph node cellular composition and function during cyclophosphamide and splenectomy induced resistance to Toxoplasma gondii

Jones

Alkan

Erb

1987

Parasite Immunology

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Murine toxoplasmosis caused by a low virulence, cyst-forming strain of Toxcoplasma gondii (Pe strain) is characterized by splenomegaly, lymphadenopathy, decreased delayed-type hypersensitivity (DTH), and the presence of toxoplasma cysts in brain tissue. Cyclophosphamide (CY) in a single dose of 100 mg/kg injected 3 days before infection, or splenectomy 3 weeks before infection, augmented DTH and decreased the number of toxoplasma brain cysts. CY-induced augmentation of resistance during the first 3 weeks of murine toxoplasmosis was associated with: (1) an increase in mononuclear phagocytes and a decrease in T lymphocytes (including Lyt2+ cells) in spleens and lymph nodes; (2) suppressed toxoplasma antigen induced proliferation of cultured spleen cells: (3) augmentation of antigen induced proliferation of cultured lymph node cells; and (4) low levels of interferon-gamma production in both spleen and lymph node cultures. The best correlate of the enhanced in-vivo effects of CY was proliferation of nylon wool-purified lymph node cells to toxoplasma antigen. The presence of Lyt2+ cells in lymph nodes of toxoplasma infected mice inhibited maximal proliferation.

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Lymphocyte Proliferative Responsiveness in 31 Patients after an Outbreak of Toxoplasmosis

Cited by 13 publications

References 0 publications

Toxoplasmosis

Toxoplasmosis

Identification of a sporozoite‐specific member of the Toxoplasma SAG superfamily via genetic complementation

Murine spleen and lymph node cellular composition and function during cyclophosphamide and splenectomy induced resistance to Toxoplasma gondii

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