Immunology for University Students
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Immunology for University Students
Resources and Material for Lecturers and Students - Immunology (University level)
Curated by Alfredo Corell
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If helper T cells have nothing to help, they kill their host

If helper T cells have nothing to help, they kill their host | Immunology for University Students |
For vaccines, CD4+ T cells can spell trouble

The ideal vaccine elicits immune memory—either antibodies or memory T cells—to protect the host from subsequent infections. T cell–mediated immunity requires both helper CD4+ T cells and cytotoxic CD8+ T cells to kill virus-infected cells. But what happens when a vaccine only elicits CD4+ memory T cells? Penaloza-MacMaster et al. probed this question by giving mice a vaccine that generated only memory CD4+ T cells against lymphocytic choriomeningitis virus (LCMV). Instead of protecting mice against chronic LCMV, vaccinated mice developed massive inflammation and died. Virus-specific CD8+ T cells or antibodies protected mice from the pathology. These results may have implications for vaccines against chronic viruses such as HIV.

Science 16 January 2015: 
Vol. 347 no. 6219 pp. 278-282 
DOI: 10.1126/science.aaa2148

Alfredo Corell's insight:

CD4 T cells promote innate and adaptive immune responses, but how vaccine-elicited CD4 T cells contribute to immune protection remains unclear. We evaluated whether induction of virus-specific CD4 T cells by vaccination would protect mice against infection with chronic lymphocytic choriomeningitis virus (LCMV). Immunization with vaccines that selectively induced CD4 T cell responses resulted in catastrophic inflammation and mortality after challenge with a persistent strain of LCMV. Immunopathology required antigen-specific CD4 T cells and was associated with a cytokine storm, generalized inflammation, and multi-organ system failure. Virus-specific CD8 T cells or antibodies abrogated the pathology. These data demonstrate that vaccine-elicited CD4 T cells in the absence of effective antiviral immune responses can trigger lethal immunopathology.

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How Salmonella inactivates the immune system

How Salmonella inactivates the immune system | Immunology for University Students |

Science 16 November 2012:
Vol. 338 no. 6109 pp. 963-967
DOI: 10.1126/science.1227037


Salmonella Inhibits Retrograde Trafficking of Mannose-6-Phosphate Receptors and Lysosome Function

Kieran McGourty1,Teresa L. Thurston1,Sophie A. Matthews1,Laurie Pinaud1,*,Luís Jaime Mota1,†,David W. Holden1,‡



Salmonella enterica is an intracellular bacterial pathogen that replicates within membrane-bound vacuoles through the action of effector proteins translocated into host cells. Salmonella vacuoles have characteristics of lysosomes but are reduced in hydrolytic enzymes transported by mannose-6-phosphate receptors (MPRs). We found that the effector SifA subverted Rab9-dependent retrograde trafficking of MPRs, thereby attenuating lysosome function. This required binding of SifA to its host cell target SKIP/PLEKHM2. Furthermore, SKIP regulated retrograde trafficking of MPRs in noninfected cells. Translocated SifA formed a stable complex with SKIP and Rab9 in infected cells. Sequestration of Rab9 by SifA-SKIP accounted for the effect of SifA on MPR transport and lysosome function. Growth of Salmonella increased in cells with reduced lysosomal activity and decreased in cells with higher lysosomal activity. These results suggest that Salmonella vacuoles undergo fusion with lysosomes whose potency has been reduced by SifA.


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Ashley Morrison's comment, August 13, 2013 12:38 PM
What are the precautions for avoiding such illnesses???