scholarly journals Antibodies to Conserved Pneumococcal Antigens Correlate with, but Are Not Required for, Protection against Pneumococcal Colonization Induced by Prior Exposure in a Mouse Model

2005 ◽  
Vol 73 (10) ◽  
pp. 7043-7046 ◽  
Author(s):  
Krzysztof Trzciński ◽  
Claudette Thompson ◽  
Richard Malley ◽  
Marc Lipsitch
Keyword(s):  
T Cells ◽  
Streptococcus Pneumoniae ◽  
Mouse Model ◽  
Prior Exposure ◽  
Correlates Of Protection ◽  
Pneumococcal Colonization

ABSTRACT In mice following intranasal exposure to Streptococcus pneumoniae, protection against pneumococcal colonization was independent of antibody but dependent on CD4+ T cells. Nonetheless, concentrations of antibodies to three conserved pneumococcal antigens correlated with protection against colonization. Concentrations of antibodies to conserved pneumococcal antigens may be correlates of protection without being effectors of protection.

scholarly journals Protection against Nasopharyngeal Colonization by Streptococcus pneumoniae Is Mediated by Antigen-Specific CD4+ T Cells

2008 ◽  
Vol 76 (6) ◽  
pp. 2678-2684 ◽  
Author(s):  
Krzysztof Trzciński ◽  
Claudette M. Thompson ◽  
Amit Srivastava ◽  
Alan Basset ◽  
Richard Malley ◽  
...  
Keyword(s):  
T Cells ◽  
Streptococcus Pneumoniae ◽  
T Cell ◽  
Protein A ◽  
Specific Antigen ◽  
Surface Protein ◽  
Bacterial Clearance ◽  
Antigen Specificity ◽  
Nasopharyngeal Colonization ◽  
Pneumococcal Colonization

ABSTRACT CD4+ T-cell-dependent acquired immunity confers antibody-independent protection against pneumococcal colonization. Since this mechanism is poorly understood for extracellular bacteria, we assessed the antigen specificity of the induction and recall of this immune response by using BALB/c DO11.10Rag−/− mice, which lack mature B and T cells except for CD4+ T cells specific for the OVA323-339 peptide derived from ovalbumin. Serotype 6B Streptococcus pneumoniae strain 603S and unencapsulated strain Rx1ΔlytA were modified to express OVA323-339 as a fusion protein with surface protein A (PspA) (strains 603OVA1 and Rx1ΔlytAOVA1) or with PspA, neuraminidase A, and pneumolysin (Rx1ΔlytAOVA3). Whole-cell vaccines (WCV) were made of ethanol-killed cells of Rx1ΔlytA plus cholera toxin (CT) adjuvant, of Rx1ΔlytAOVA1 + CT (WCV-OVA1), and of Rx1ΔlytAOVA3 + CT (WCV-OVA3). Mice intranasally immunized with WCV-OVA1, but not with WCV or CT alone, were protected against intranasal challenge with 603OVA1. There was no protection against strain 603S in mice immunized with WCV-OVA1. These results indicate antigen specificity of both immune induction and the recall response. Effector action was not restricted to antigen-bearing bacteria since colonization by 603S was reduced in animals immunized with vaccines made of OVA-expressing strains when ovalbumin or killed Rx1ΔlytAOVA3 antigen was administered around the time of challenge. CD4+ T-cell-mediated protection against pneumococcal colonization can be induced in an antigen-specific fashion and requires specific antigen for effective bacterial clearance, but this activity may extend beyond antigen-expressing bacteria. These results are consistent with the recruitment and/or activation of phagocytic or other nonspecific effectors by antigen-specific CD4+ T cells.

scholarly journals Infant Mouse Model for the Study of Shedding and Transmission during Streptococcus pneumoniae Monoinfection

2016 ◽  
Vol 84 (9) ◽  
pp. 2714-2722 ◽  
Author(s):  
M. Ammar Zafar ◽  
Masamitsu Kono ◽  
Yang Wang ◽  
Tonia Zangari ◽  
Jeffrey N. Weiser
Keyword(s):  
Streptococcus Pneumoniae ◽  
Mouse Model ◽  
Influenza A ◽  
Carrier State ◽  
High Ratio ◽  
New Host ◽  
Content Type ◽  
Infant Mouse ◽  
Colonization Density ◽  
Pneumococcal Colonization

One of the least understood aspects of the bacteriumStreptococcus pneumoniae(pneumococcus) is its transmission from host to host, the critical first step in both the carrier state and the disease state. To date, transmission models have depended on influenza A virus coinfection, which greatly enhances pneumococcal shedding to levels that allow acquisition by a new host. Here, we describe an infant mouse model that can be utilized to study pneumococcal colonization, shedding, and transmission during bacterial monoinfection. Using this model, we demonstrated that the level of bacterial shedding is highest in pups infected intranasally at age 4 days and peaks over the first 4 days postchallenge. Shedding results differed among isolates of five different pneumococcal types. Colonization density was found to be a major factor in the level of pneumococcal shedding and required expression of capsule. Transmission within a litter occurred when there was a high ratio of colonized “index” pups to uncolonized “contact” pups. Transmission was observed for each of the well-colonizing pneumococcal isolates, with the rate of transmission proportional to the level of shedding. This model can be used to examine bacterial and host factors that contribute to pneumococcal transmission without the effects of viral coinfection.

Resident memory and recirculating memory T cells cooperate to maintain disease in a mouse model of vitiligo

immuneACCESS ◽  
2018 ◽  
Author(s):  
JM Richmond ◽  
JP Strassner ◽  
M Rashighi ◽  
P Agarwal ◽  
M Garg ◽  
...  
Keyword(s):  
T Cells ◽  
Mouse Model ◽  
Memory T Cells

Tanshinone IIA alleviates vitiligo by suppressing AKT mediated CD8 + T cells activation in a mouse model

2021 ◽  
Author(s):  
Diancai Zhang ◽  
Yujie Wang ◽  
Guangzhi Li ◽  
Baoxiang Zhang
Keyword(s):  
T Cells ◽  
Mouse Model ◽  
Cd8 T Cells ◽  
Tanshinone Iia

scholarly journals Single-cell evaluation reveals shifts in the tumor-immune niches that shape and maintain aggressive lesions in the breast

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Vidya C. Sinha ◽  
Amanda L. Rinkenbaugh ◽  
Mingchu Xu ◽  
Xinhui Zhou ◽  
Xiaomei Zhang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
T Cells ◽  
Mouse Model ◽  
Transition State ◽  
Tumor Cell ◽  
Single Cell ◽  
Tumor Cells ◽  
Breast Lesions ◽  
Aggressive Tumor ◽  
Insight Into

AbstractThere is an unmet clinical need for stratification of breast lesions as indolent or aggressive to tailor treatment. Here, single-cell transcriptomics and multiparametric imaging applied to a mouse model of breast cancer reveals that the aggressive tumor niche is characterized by an expanded basal-like population, specialization of tumor subpopulations, and mixed-lineage tumor cells potentially serving as a transition state between luminal and basal phenotypes. Despite vast tumor cell-intrinsic differences, aggressive and indolent tumor cells are functionally indistinguishable once isolated from their local niche, suggesting a role for non-tumor collaborators in determining aggressiveness. Aggressive lesions harbor fewer total but more suppressed-like T cells, and elevated tumor-promoting neutrophils and IL-17 signaling, disruption of which increase tumor latency and reduce the number of aggressive lesions. Our study provides insight into tumor-immune features distinguishing indolent from aggressive lesions, identifies heterogeneous populations comprising these lesions, and supports a role for IL-17 signaling in aggressive progression.

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