Jack Gorski

C-terminal anchoring of a peptide to class II MHC via the P10 residue is compatible with a peptide bulge.

Overlap of direct and indirect alloreactive T-cell repertoires when MHC polymorphism is limited to the peptide binding groove.

A molecular marker for thymocyte-positive selection: selection of CD4 single-positive thymocytes with shorter TCRB CDR3 during T cell development.

Re-establishing peripheral tolerance in the absence of CTLA-4: complementation by wild-type T cells points to an indirect role for CTLA-4.

Evidence for preferred MHC class II-TCR recognition independent of the source of bound peptide.

Elimination of leukemia in the absence of lethal graft-versus-host disease after allogenic bone marrow transplantation.

A fractal clonotype distribution in the CD8+ memory T cell repertoire could optimize potential for immune responses.

T cell receptor CDR3 loop length repertoire is determined primarily by features of the V(D)J recombination reaction.

Cutting edge: TCR contacts as anchors: effects on affinity and HLA-DM stability.

Selective elimination of alloreactive donor T cells attenuates graft-versus-host disease and enhances T-cell reconstitution.

Gamma delta T cell regulation of IFN-gamma production by central nervous system-infiltrating encephalitogenic T cells: correlation with recovery from experimental autoimmune encephalomyelitis.

A polymorphic pocket at the P10 position contributes to peptide binding specificity in class II MHC proteins.

Cooperativity during the formation of peptide/MHC class II complexes.

Factor VIII ectopically targeted to platelets is therapeutic in hemophilia A with high-titer inhibitory antibodies.

Complex T cell memory repertoires participate in recall responses at extremes of antigenic load.

Homeostatic expansion and repertoire regeneration of donor T cells during graft versus host disease is constrained by the host environment.

Cooperativity of hydrophobic anchor interactions: evidence for epitope selection by MHC class II as a folding process.

Crystallographic structure of the human leukocyte antigen DRA, DRB3*0101: models of a directional alloimmune response and autoimmunity.

Quantitative measurement of pathogen-specific human memory T cell repertoire diversity using a CDR3 beta-specific microarray.

Long-term results of bone marrow transplantation in complete DiGeorge syndrome.

Impaired survival of peripheral T cells, disrupted NK/NKT cell development, and liver failure in mice lacking Gimap5.

HLA-DM mediates epitope selection by a "compare-exchange" mechanism when a potential peptide pool is available.

An accessible micro-capillary electrophoresis device using surface-tension-driven flow.

A clonotype nomenclature for T cell receptors.

The transcription factor RFX protects MHC class II genes against epigenetic silencing by DNA methylation.

Two compensatory pathways maintain long-term stability and diversity in CD8 T cell memory repertoires.

Peptide-MHC class II complex stability governs CD4 T cell clonal selection.

Cutting edge: HLA-DM-mediated peptide exchange functions normally on MHC class II-peptide complexes that have been weakened by elimination of a conserved hydrogen bond.

Phospholipase C{gamma}1 is essential for T cell development, activation, and tolerance.

Simulation studies for a multistage dynamic process of immune memory response to influenza: experiment in silico.

Disproportional effects in populations of concern for pandemic influenza: insights from seasonal epidemics in Wisconsin, 1967-2004.

Functional dichotomy between NKG2D and CD28-mediated co-stimulation in human CD8+ T cells.

Naive T cell repertoire skewing in HLA-A2 individuals by a specialized rearrangement mechanism results in public memory clonotypes.

Selective T cell expansion during aging of CD8 memory repertoires to influenza revealed by modeling.

The polyclonal CD8 T cell response to influenza M158-66 generates a fully connected network of cross-reactive clonotypes to structurally related peptides: a paradigm for memory repertoire coverage of novel epitopes or escape mutants.

A requisite role for induced regulatory T cells in tolerance based on expanding antigen receptor diversity.