Bibliography
- OLSSON T Critical influences of the cytokine orches- tration on the outcome of myelin- antigen-specific T-cell autoimmunity in experimental autoimmune encephalomyelitis and multiple scleroris. Immunol Rev. (1995) 144:245–268.
- •Provides a summary of the role of cytokines and T-cell proliferation factors in autoimmune disease.
- BERRIDGE MJ: Lymphocyte activation in health and disease. Grit. Rev. Immunol. (1997) 17:155-178. See reference [1] for annotation.
- MARTIN R, MACFARLAND HF: Immunological aspects of experimental allergic encephalomyelitis and multiple sclerosis. Grit. Rev. Clin. Lab. Sci. (1995) 32:121-182. A comprehesive review of the data on fine-specificity, V-gene usage, precursor frequencies and cytokine profiles of human myelin-specific T-cells.
- VANDEVYVER C, MOTMANS K, STINISSEN P, ZHANG J, RAUS J: Cytokine mRNA profile of myelin basic protein reactive T-cell clones in patients with multiple sclerosis. Autoimm unity (1998) 28:77–89.
- •Provides additional data on very similar cytokine responses of MBP-specific T-cells in MS patients and control.
- WINDHAGEN A, ANDERSON DE, CARRIZOSA A, BALASHOV K, WEINER HL, HAFLER DA: Cytokine secretion of myelin basic protein reactive T cells in patients with multiple sclerosis. J. Neuroimmunol (1998) 91:1–9.
- •See reference [4] for annotation.
- BURNS J, BARTHOLOMEW B, LOBO S: Isolation of myelin basic protein-specific T cells predominantly from the memory T-cell compartment in multiple sclerosis. Ann. Neurol (1999) 45:33–39.
- •Presents novel data from four different approaches that MBP-specific memory T-cells are more frequent in MS patients than in healthy controls.
- ILLES Z, KONDO T, YOKOYAMA K, OHASHI T, TABIRA T, YAMAMURA T: Identification of autoimmune T cells among in vivo expanded CD25+ T cells in multiple sclerosis. J. Immunol (1999) 162:1811–1817.
- •See reference [6] for annotation.
- LOVETT-RACKE A, TROTTER JL, LAUBER J, PERRIN PJ, JUNE CH, RACKE MK: Decreased dependence of myelin basic protein-reactive T cells on CD28-mediated costimulation in multiple sclerosis patients. J. Clin. Invest. (1998) 101:725–730.
- •See reference [6] for annotation.
- SCHOLZ C, PATTON KT, ANDERSON DE, FREEMAN GJ, HAFLER DA: Expansion of autoreactive T cells in multiple sclerosis is independent of exogenous B7 costimulation. j Immunol (1998) 160:1532–1538.
- •See reference [6] for annotation.
- VAN NOORT JM, VAN SECHEL AC, BAJRAMOVIC JJ et al: The small stress protein alpha B-crystallin as candidate autoantigen in multiple sclerosis. Nature (1995) 375:798–801.
- ••A study that for the first time compares the relative immuno-genicity of the complete collection of myelin antigens to human T-cells and identifies a B-crystallin as an immuno-dominant myelin antigen.
- LEHMANN PV, FORSTHUBER T, MILLER A, SERCARZ EE: Spreading of T-cell autoimmunity to cryptic determi-nants of an autoantigen. Nature (1992) 358:155–157.
- •Documents the now generally accepted phenomenon of determinant spreading.
- MCRAE BL, VADERLUGT CL, DAL CANTO MC, MILLER SD: Functional evidence for epitope spreading in the relapsing pathology of experimental autoimmune encephalomyelitis. J. Exp. Med. (1995) 182:75–85.
- •See reference [11] for annotation.
- YU M, JOHGNSON JM, TUOHY VK: A predictable sequen- tial determinant spreading cascade invariably accompanies progression of experimental autoim-mune encephalomyelitis: a basis for peptide-specific therapy after onset of clinical disease. J. Exp. Med. (1996) 183:1777–1788.
- •See reference [11] for annotation.
- TUOHY VK, YU M, YIN L, KAWCZAK JA, KINKEL RP: Spontaneous regression of primary autoreactivity during chronic progression of experimental autoim-mune encephalomyelitis and multiple sclerosis. J. Exp. Med. (1999) 189:1033–1042.
- •A study that demonstrates down regulation of myelin-specific T-cell responses in mice and humans.
- SALVETTI M, RISTORI G, D'AMATO M et al: Predominant and sTable T cell responses to regions of myelin basic protein can be detected in individuals with multiple sclerosis. Eur. j Immunol (1993) 23:1232–1239.
- •Provides independent evidence for the existence of relatively stable T-cell responses to MBP determinants in established MS.
- MEINL E, WEBER F, DREXLER K et al.: Myelin basic protein-specific T lymphocyte repertoire in multiple sclerosis. Complexity of the response and dominance of nested epitopes due to recruitment of multiple T-cell clones. J. Olin. Invest. (1993) 92:2633–2643.
- •See reference [15] for annotation.
- WUCHERPFENNIG KW, ZHANG J, WITEK C et al.: Clonal expansion and persistence of human T cells specific for an immunodominant myelin basic protein. J. Immunol. (1994) 152:5581–5592.
- •See reference [15] for annotation.
- UCELLI A, GIUNTI D, SALVETTI M et al: A restricted T-cell response to myelin basic protein (MBP) is sTable in multiple sclerosis (MS) patients. Olin. Exp. Immunol (1998) 111:186–192.
- •See reference [15] for annotation.
- LENARDO M, CHAN KM, HORNUNG F et al: Mature T lymphocyte apopotosis - immune regulation in a dynamic and unpredictable antigenic environment. Ann. Rev. Immunol (1999) 17:221–253.
- ••A review on mechanisms that control peripheral responsive-ness to self-antigens.
- SPRENT J, TOUGH DF, SUN S: Factors controlling the turnover of T memory cells. Immunol. Rev. (1997) 156:79–85.
- ••Provides updated important views on the generation andmaintenance of memory T-cells.
- ZINKERNAGEL RM, EHL S, AICHELE P, OEHEN S, KUNDIG T, HERNGARTNER H: Antigen localisation regulates immune responses in a dose-and time-dependent fashion: a geographical view of immune reactivity. Immunol. Rev. (1997) 156:199–209.
- ••See reference [20] for annotation.
- DUTTON RW, SWAIN SL, BRADLEY LM: The generation and maintenance of memory T and B-cells. Immunol Today (1999) 20:291–293.
- ••See reference [20] for annotation.
- FORSTER I, LIEBERAM I: Peripheral tolerance of CD4 Tcells following local activation in adolescent mice. Eur. Immunol (1996) 26:3194–3202.
- ADLER AJ, MARSH DW, YOCHUM GS et al: CD4+ T-celltolerance to parenchymal self-antigens requires presentation by bone marrow-derived antigen-presenting cells. J. Exp. Med. (1998) 187:1555–1564.
- •Presents data to indicate how normal presentation pathways can be used not only for T-cell priming, but also for T-cell tolerisation.
- VAN PARIJS L, PETERSON DA, ABBAS AK: The fas/fas ligand pathway and bc1-2 regulate T-cell responses to model self and foreign antigens. Immunity (1998) 8:265–274.
- •See reference [24] for annotation.
- HEATH WR, KURTS C, MILLER JFAP, CARBONE FR: Cross- tolerance: a pathway for inducing tolerance to periph-eral tissue antigens. J. Exp. Med. (1998) 187:1549–1553.
- •See reference [24] for annotation.
- VAN DE KEERE F, TONEGAWA S: CD4(+) T cells prevent spontaneous experimental autoimmune encephalo-myelitis in anti-myelin basic protein T cell receptor transgenic mice. J. Exp. Med. (1998) 188:1875–1882.
- •An elegant study demonstrating control of autoreactive T-cells by other T-cells.
- VAN SECHEL AC, BAJRAMOVIC JJ, VAN STIPDONK MJB, PERSOON-DEEN C, GEUTSKENS SB, VAN NOORT JM: EBV-induced expression and HLA-DR-restricted presentation by human B cells of aB-crystallin, a candidate autoantigen in multiple sclerosis. J. Immunol (1999) 162:129–135.
- •A study showing how peripheral viral infection can lead to T-cell presentation of a myelin protein that is otherwise absent from the lymphoid compartment, a mechanism unique to humans.
- GARCIA KC, TEYTON L, WILSON IA: Structural basis ofT-cell recognition. Ann. Rev. Immunol. (1999) 17: 369–297.
- SLOAN-LANCASTER J, ALLEN PM: Altered peptideligand-induced partial T-cell activation: molecular mechanisms and role in T-cell biology. Ann. Rev. Immunol. (1996) 14:1–27.
- HEMMER B, VERGELLI M, GRAN B et al: Predictable TCR antigen recognition based on peptide scans leads to the identification of agonist ligands with no sequence homology. J. Immunol (1998) 160:3631–3636.
- ••This study reveals the surprising degree of cross-reactivity ofTCRs that allows responses by a single T-cell to apparently fully unrelated amino acid sequences.
- MASON D: A very high level of crossreactivity is an essential feature of the T-cell receptor. Immunol Today (1998) 19:395–404.
- ••An intriguing view that explains the functionality of a highlevel of TCR cross-reactivity.
- BROCK R, WIESMULLER KH, JUNG G, WALDEN P: Molecular basis for the recognition of two structurally different major histocompatibility complex/peptide complexes by a single T-cell receptor. Proc. Natl. Acad. Sci. USA (1996) 93:13108–13113.
- •Presents examples where TCRs display a surprising degree of cross-reactivity and plasticity.
- AUSUBEL LJ, KWAN CK, SETTE A, KUCHROO VK, HAFLER DA: Complementary mutations in an antigenic peptide allow for crossreactivity of autoreactive T-cell clones. Proc. Natl. Acad. Sci. USA (1996) 93:15317–15322.
- •See reference [33] for annotation.
- LOFTUS C, HUSEBY E, GOPAUL P, BEESON C, GOVERMAN J: Highly cross-reactive T-cell responses to myelin basic protein epitopes reveal a nonpredictable form of TCR degeneracy. J. Immunol. (1999) 162:6451–6457.
- •See reference [33] for annotation.
- NICHOLSON LB, MURTAZA A, HAFLER BP, SETTE A, KUCHROO VK: A T cell receptor antagonist peptide induces T cells that mediate bystander suppression and prevent autoimmune encephalomyelitis induced with multiple myelin antigens. Proc. Natl. Acad. Sci. USA (1998) 94:9279–9284.
- •An example of the therapeutic potential of APL, even in disease mediated by multiple myelin-specificities.
- BROCKE S, GIJBELS K, ALLEGRETTA et al.: Treatment of experimental encephalomyelitis with a peptide analogue of myelin basic protein. Nature (1996) 279:343–345.
- •A study that shows how APL can down regulate experi-mental disease by triggering IL-4 production of only a few cells involved in the inflammatory infiltrate in EAE.
- ANDERTON SM, MANICKASINGHAM SP, BURKHART C et al.: Fine specificity of the myelin-reactive T cell repertoire: implications for TCR antagonism in autoimmunity. j Immunol (1998) 161:3357–3364.
- •This study reveals how unpredictable the in vivo effects of APL may turn out to be.
- KOZOVSKA M, ZANG Y, AEBISHER I et al.: T cell recogni- tion motifs of an immunodominant peptide of myelin basic protein in patients with multiple sclerosis: structural requirements and clinical implications. Eur. Immunol (1998) 28:1894–1901.
- •An example of how defined APLs can have widely differin effects on different T-cells that are reactive to the same MBP epitope.
- ACHA-ORBEA H, MITCHELL DJ, TIMMERMANN L et al: Limited heterogeneity of T-cell recptors from lympho-cytes mediating autoimmune encephalomyelitis allows specific immune intervention. Cell (1988) 54:263–273.
- BURNS FR, LI XB, SHEN N eta].: Both rat and mouse T-cellreceptors specific for the encephalitogenic determi-nant of myelin basic protein use similar V a and V 13 chain genes even though the major histocompatibility complex and encephalitogenic determinants being recognised are different. J. Exp. Med. (1989) 169:27–39.
- FUJINAMI RS, OLDSTONE MB: Amino acid homology between the encephalitogenic site of myelin basic protein and virus: mechanism for autoimmunity. Science (1985) 230:1043–1045.
- WUCHERPFENNIG KW, STROMINGER JL: Molecular mimicry in T cell-mediated autoimmunity: viral peptides activate human T-cell clones specific for myelin basic protein. Cell (1995) 80:695–705.
- •Reveals the surprisingly large domain of molecular mimicry by showing how microbial peptides with sometimes very limited sequence homology to an MBP determinant can still activate MBP-specific T-cells.
- HAUSMANN S, MARTIN M, GAUTHIER L, WUCHERPFENNIG KW: Structural features of autoreac-tive TCR that determine the degree of degeneracy in peptide recognition. J. Immunol (1999) 162:338–344.
- •See reference [43] for annotation.
- CHEN Y, INOBE J, MARKS R, GONNELLA P, KUCHROO VK, WEINER HL: Peripheral deletion of antigen-reactive T cells in oral tolerance. Nature (1995) 376: 177–180.
- •Shows the potential of antigen-specific oral tolerance induction.
- BENSON JM, STUCKMAN SS, COX KL et al: Oral admini- stration of myelin basic protein is superior to myelin in suppressing established relapsing experimental autoimmune encephalomyelitis. J. Immunol (1999) 162: 6247–6254.
- •See reference [45] for annotation.
- METZLER B, WRAITH DC: Inhibition of experimental autoimmune encephalomyelitis by inhalation but not oral administration of encephalitogenic peptide: influence of MHC binding affinity. mt. Immunol (1993) 5:1159–1165.
- •Illustrates how antigen can be administered in order to establish immunological tolerance.
- LIBLAU RS, TISCH R, SHOKAT K et al.: Intravenous injection of soluble antigen induces thymic and peripheral T-cell apoptosis. Proc. Natl. Acad. Sci. USA (1996) 93:3031–3036.
- •See reference [47] for annotation.
- RACKE MK, CRITCHFIELD JM, QUIGLEY L et al: Intrave- nous antigen administration as a therapy for autoim-mune demyelinating disease. Ann. Neurol (1996) 39: 46–56.
- •See reference [47] for annotation. Johannes M van Noort