scholarly journals From antibody specificity to T cell recognition

2021 ◽  
Vol 218 (4) ◽  
Author(s):  
Hye-Jung Kim ◽  
Harvey Cantor
Keyword(s):  
Public Health ◽  
Blood Transfusion ◽  
Human Genetics ◽  
Clonal Selection ◽  
Immune Recognition ◽  
Antibody Specificity ◽  
Cell Recognition ◽  
T Cell Recognition ◽  
Self Tolerance ◽  
Definition Of

Landsteiner’s definition of human blood groups and the genetic rules that govern blood transfusion represents a milestone in human genetics and a historic event in public health. His research into the specificity of serological reactions, although less well known, has had a critical influence on the development of contemporary views on immune recognition, clonal selection, and immunological self-tolerance.

scholarly journals Conformation-dependent recognition of a protein by T cells requires presentation without processing

1989 ◽  
Vol 259 (3) ◽  
pp. 731-735 ◽  
Author(s):  
M Z Atassi ◽  
G S Bixler ◽  
T Yokoi
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cell Lines ◽  
Protein Antigen ◽  
Mouse Strains ◽  
Immune Recognition ◽  
Cell Recognition ◽  
T Cell Recognition ◽  
T Cell Lines

Presentation of a protein antigen to T cells is believed to follow its intracellular breakdown by the antigen-presenting cell, with the fragments constituting the trigger of immune recognition. It should then be expected that T-cell recognition of protein antigens in vitro will be independent of protein conformation. Three T-cell lines were made by passage in vitro with native lysozyme of T cells from two mouse strains (B10.BR and DBA/1) that had been primed with the same protein. These cell lines responded well to native lysozyme and very poorly to unfolded (S-sulphopropyl) lysozyme. The response of the T-cell lines to the antigen was major histocompatibility complex (MHC)-restricted. A line from B10.BR was selected for further studies. This line responded to the three surface-simulation synthetic sites of lysozyme (representing the discontinuous antigenic, i.e. antibody binding, sites) and analogues that were extended to a uniform size by a nonsense sequence. T-cell clones prepared from this line were specific to native lysozyme and did not respond to the unfolded derivative. Furthermore, several of these clones showed specificity to a given surface-simulation synthetic site. The exquisite dependency of the recognition by the clones on the conformation of the protein antigen and their ability to recognize the surface-simulation synthetic sites indicate that the native (unprocessed) protein was the trigger of MHC-restricted T-cell recognition.

scholarly journals T-Cell Tolerance for Variability in an HLA Class I-Presented Influenza A Virus Epitope

2009 ◽  
Vol 83 (18) ◽  
pp. 9206-9214 ◽  
Author(s):  
Angela Wahl ◽  
William McCoy ◽  
Fredda Schafer ◽  
Wilfried Bardet ◽  
Rico Buchli ◽  
...  
Keyword(s):  
Influenza Virus ◽  
T Cell ◽  
Influenza A Virus ◽  
Influenza A ◽  
Viral Escape ◽  
Class I ◽  
Immune Recognition ◽  
Cell Recognition ◽  
T Cell Recognition ◽  
The Impact

ABSTRACT To escape immune recognition, viruses acquire amino acid substitutions in class I human leukocyte antigen (HLA)-presented cytotoxic T-lymphocyte (CTL) epitopes. Such viral escape mutations may (i) prevent peptide processing, (ii) diminish class I HLA binding, or (iii) alter T-cell recognition. Because residues 418 to 426 of the hypervariable influenza A virus nucleoprotein (NP418-426) epitope are consistently bound by class I HLA and presented to CTL, we assessed the impact that intraepitope sequence variability has upon T-cell recognition. CTL elicited by intranasal influenza virus infection were tested for their cross-recognition of 20 natural NP418-426 epitope variants. Six of the variant epitopes, of both H1N1 and H3N2 origin, were cross-recognized by CTL while the remaining NP418-426 epitope variants escaped targeting. A pattern emerged whereby variability at position 5 (P5) within the epitope reduced T-cell recognition, changes at P4 or P6 enabled CTL escape, and a mutation at P8 enhanced T-cell recognition. These data demonstrate that substitutions at P4 and/or P6 facilitate influenza virus escape from T-cell recognition and provide a model for the number, nature, and location of viral mutations that influence T-cell cross-recognition.

scholarly journals Structurally silent peptide anchor modifications allosterically modulate T cell recognition in a receptor-dependent manner

2021 ◽  
Vol 118 (4) ◽  
pp. e2018125118
Author(s):  
Angela R. Smith ◽  
Jesus A. Alonso ◽  
Cory M. Ayres ◽  
Nishant K. Singh ◽  
Lance M. Hellman ◽  
...  
Keyword(s):  
T Cell ◽  
Immune Responses ◽  
Class I ◽  
Immune Recognition ◽  
Dependent Manner ◽  
Cell Recognition ◽  
Class I Mhc ◽  
T Cell Recognition ◽  
Modified Peptides ◽  
The Impact

Presentation of peptides by class I MHC proteins underlies T cell immune responses to pathogens and cancer. The association between peptide binding affinity and immunogenicity has led to the engineering of modified peptides with improved MHC binding, with the hope that these peptides would be useful for eliciting cross-reactive immune responses directed toward their weak binding, unmodified counterparts. Increasing evidence, however, indicates that T cell receptors (TCRs) can perceive such anchor-modified peptides differently than wild-type (WT) peptides, although the scope of discrimination is unclear. We show here that even modifications at primary anchors that have no discernible structural impact can lead to substantially stronger or weaker T cell recognition depending on the TCR. Surprisingly, the effect of peptide anchor modification can be sensed by a TCR at regions distant from the site of modification, indicating a through-protein mechanism in which the anchor residue serves as an allosteric modulator for TCR binding. Our findings emphasize caution in the use and interpretation of results from anchor-modified peptides and have implications for how anchor modifications are accounted for in other circumstances, such as predicting the immunogenicity of tumor neoantigens. Our data also highlight an important need to better understand the highly tunable dynamic nature of class I MHC proteins and the impact this has on various forms of immune recognition.

Peri-urban water, sanitation and hygiene in Lusaka, Zambia: photovoice empowering local assessment via ecological theory

2021 ◽  
pp. 175797592199571
Author(s):  
Sikopo Nyambe ◽  
Taro Yamauchi
Keyword(s):  
Public Health ◽  
Public Policy ◽  
Health Hazard ◽  
Disease Outbreaks ◽  
Ecological Theory ◽  
Urban Slum ◽  
Health Concern ◽  
Minimal Impact ◽  
Sanitation And Hygiene ◽  
Definition Of

Water, sanitation and hygiene (WASH) factors are responsible for 11.4% of deaths in Zambia, making WASH a key public health concern. Despite annual waterborne disease outbreaks in the nation’s peri-urban (slum) settlements being linked to poor WASH, few studies have proactively analysed and conceptualised peri-urban WASH and its maintaining factors. Our study aimed to (a) establish residents’ definition of peri-urban WASH and their WASH priorities; and (b) use ecological theory to analyse the peri-urban WASH ecosystem, highlighting maintaining factors. Our study incorporated 16 young people (aged 17–24) residing in peri-urban Lusaka, Zambia in a photovoice exercise. Participants took photographs answering the framing question, ‘What is WASH in your community?’ Then, through contextualisation and basic codifying, participants told the stories of their photographs and made posters to summarise problems and WASH priorities. Participant contextualisation and codifying further underwent theoretical thematic analysis to pinpoint causal factors alongside key players, dissecting the peri-urban WASH ecosystem via the five-tier ecological theory ranging from intrapersonal to public policy levels. Via ecological theory, peri-urban WASH was defined as: (a) poor practice (intrapersonal, interpersonal); (b) a health hazard (community norm); (c) substandard and unregulated (public policy, organisational); and (d) offering hope for change (intrapersonal, interpersonal). Linked to these themes, participant findings revealed a community level gap, with public policy level standards, regulations and implementation having minimal impact on overall peri-urban WASH and public health due to shallow community engagement and poor acknowledgement of the WASH realities of high-density locations. Rather than a top-down approach, participants recommended increased government–resident collaboration, offering residents more ownership and empowerment for intervention, implementation and defending of preferred peri-urban WASH standards.

scholarly journals Topoisomerase inhibitors modulate expression of melanocytic antigens and enhance T cell recognition of tumor cells

2010 ◽  
Vol 60 (1) ◽  
pp. 133-144 ◽  
Author(s):  
Timothy J. Haggerty ◽  
Ian S. Dunn ◽  
Lenora B. Rose ◽  
Estelle E. Newton ◽  
Sunil Martin ◽  
...  
Keyword(s):  
T Cell ◽  
Tumor Cells ◽  
Cell Recognition ◽  
Topoisomerase Inhibitors ◽  
T Cell Recognition

scholarly journals Cell-mediated lympholysis to H-2-matched target cells modified with a series of nitrophenyl compounds.

1976 ◽  
Vol 144 (4) ◽  
pp. 1134-1140 ◽  
Author(s):  
T G Rehn ◽  
J K Inman ◽  
G M Shearer
Keyword(s):  
T Cell ◽  
Target Cells ◽  
Cell Recognition ◽  
Receptor Model ◽  
Spleen Cells ◽  
Effector Cells ◽  
T Cell Recognition ◽  
Cytotoxic Effector

The specificity of C57BL/10 cytotoxic effector cells generated by in vitro sensitization with autologous spleen cells modified with a series of related nitrophenyl compounds was investigated. The failure of trinitrophenyl (TNP)-sensitized effector cells to lyse TNP-beta-alanylglycylglycyl(AGG)-modified target cells is presented as evidence contradicting the intimacy or dual receptor model or T-cell recognition in its simplest form. Data are also shown indicating that sensitization with N-(3-nitro-4-hydroxy-5-iodophenylacetyl)-AGG-modified stimulating cells generates noncross-reacting clones of cytotoxic effector cells.

T CELL RECOGNITION IN AUTOIMMUNE DISEASE

1993 ◽  
Vol 23 (s1) ◽  
pp. 11-11
Author(s):  
Paul J Fairchild ◽  
David C Wraith
Keyword(s):  
T Cell ◽  
Autoimmune Disease ◽  
Cell Recognition ◽  
T Cell Recognition
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