Thymus Dependence of Resistance to Infection with Babesia microti of Human Origin in Mice

Ruebush, Mary J.; Hanson, William L.

doi:10.4269/ajtmh.1980.29.507

Cited by 36 publications

(18 citation statements)

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“…In contrast, SCID mice developed a severe chronic parasitemia that fluctuated around 40%. TCR␣␤-deficient mice yielded a parasitemia curve indistinguishable from that of SCID mice; this is consistent with previous studies that have demonstrated a critical role for T cells, particularly CD4 ϩ T cells, in clearing B. microti in mice (6,13,21). IFN-␥ knockout mice consistently developed parasitemias less severe than those of SCID mice yet significantly greater than those of wild-type controls.…”

supporting

confidence: 79%

“…A better understanding of the immune response to babesial infection could be helpful in designing a safe and efficacious vaccine. While previous reports on mice have shown a strong role for T cells and the Th1 cytokine gamma interferon (IFN-␥) in the control of B. microti infection (6,13,21), results regarding the role of humoral immunity in parasite clearance have been less clearcut (2,4,13). In this study, we mouse adapted a freshly obtained B. microti clinical isolate in order to clarify the contributions of cellular and humoral immunity to disease resolution in a murine model.…”

mentioning

confidence: 82%

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Cellular Immunity, but Not Gamma Interferon, Is Essential for Resolution ofBabesia microtiInfection in BALB/c Mice

Clawson

Paciorkowski²,

Rajan³

et al. 2002

Infect Immun

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A new strain of Babesia microti (KR-1) was isolated from a Connecticut resident with babesiosis by hamster inoculation and adapted to C3H/HeJ and BALB/c mice. To examine the relative importance of humoral and cellular immunity for the control of B. microti infection, we compared the course of disease in wild-type BALB/c mice with that in BALB/c SCID mice, JHD-null (B-cell-deficient) mice, and T-cell receptor ␣␤ (TCR␤ ؊/؊ ) or gamma interferon (IFN-␥) (IFN-␥ ؊/؊ ) knockout mice following inoculation with the KR-1-strain. SCID mice and TCR␣␤ knockouts sustained a severe but nonlethal parasitemia averaging 35 to 45% infected erythrocytes. IFN-␥-deficient mice developed a less severe parasitemia but were able to clear the infection. In contrast, in six of eight JHD-null mice, the levels of parasitemia were indistinguishable from those in the wild-type animals. These data indicate that cellular immunity is critical for the clearance of B. microti in BALB/c mice but that disease resolution can occur even in the absence of IFN-␥.

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confidence: 79%

mentioning

confidence: 82%

Cellular Immunity, but Not Gamma Interferon, Is Essential for Resolution ofBabesia microtiInfection in BALB/c Mice

Clawson

Paciorkowski²,

Rajan³

et al. 2002

Infect Immun

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“…Infecting congenically athymic mice (36,193) with B. microti results in an elevated persistent parasitemia, which contrasts with the transient parasitemia observed in normal mice. These data indicate that the T cells are critical in resistance to babesiosis and also that the T-cellmediated mechanisms occur at the resolution stage (193).…”

Section: Host Immune Responsementioning

confidence: 53%

Babesiosis

Homer¹,

Aguilar-Delfín²,

Telford³

et al. 2000

Clinical Microbiology Reviews

520

402

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“…Using a clinical isolate maintained in ticks, we observed that DBA/2 mice develop an intense but transient parasitemia, whereas C57BL/6 and BALB/c mice present a marginal parasitemia. Using scid mice which lack T and B lymphocytes, we confirmed that adaptive immunity is required for a sustained resistance to babesiosis in BALB/c mice (22,28). In the present study, we used these models of B. microti infection to examine the contribution of reticulocytes and erythrocytes to the parasite burden.…”

mentioning

confidence: 99%

Babesia microti Primarily Invades Mature Erythrocytes in Mice

et al. 2006

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Babesia microti is a tick-borne red blood cell parasite that causes babesiosis in people. Its most common vertebrate reservoir is the white-footed mouse. To determine whether B. microti invades reticulocytes, as does the canine pathogen B. gibsoni, we infected the susceptible inbred mouse strains C.B-17.scid and DBA/2 with a clinical isolate of B. microti. Staining of fixed permeabilized red blood cells with 4,6-diamidino-2-phenylindole or YOYO-1, a sensitive nucleic acid stain, revealed parasite nuclei as large bright dots. Flow cytometric analysis indicated that parasite DNA is primarily found in mature erythrocytes that expressed Babesia antigens but not the transferrin receptor CD71. In contrast, CD71-positive reticulocytes rarely contained Babesia nuclei and failed to express Babesia antigens. Accordingly, the frequency of YOYO-1-positive, CD71-negative cells strongly correlated with parasitemia, defined as the frequency of infected red blood cells assessed on Giemsastained blood smears. Importantly, the absolute numbers generated by the two techniques were similar. Parasitemia was modest and transient in DBA/2 mice but intense and sustained in C.B-17.scid mice. In both strains, parasitemia preceded reticulocytosis, but reticulocytes remained refractory to B. microti. In immunocompetent C.B-17 mice, reticulocytosis developed early, despite a marginal and short-lived parasitemia. Likewise, an early reticulocytosis developed in resistant BALB/cBy and B10.D2 mice. These studies establish that B. microti has a tropism for mature erythrocytes. Although reticulocytes are rarely infected, the delayed reticulocytosis in susceptible strains may result from parasite or host activities to limit renewal of the mature erythrocyte pool, thereby preventing an overwhelming parasitemia.

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Thymus Dependence of Resistance to Infection with Babesia microti of Human Origin in Mice

Cited by 36 publications

References 0 publications

Cellular Immunity, but Not Gamma Interferon, Is Essential for Resolution ofBabesia microtiInfection in BALB/c Mice

Cellular Immunity, but Not Gamma Interferon, Is Essential for Resolution ofBabesia microtiInfection in BALB/c Mice

Babesiosis

Babesia microti Primarily Invades Mature Erythrocytes in Mice

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