scholarly journals Non-specific peptide size effects in the recognition by site-specific T-cell clones. Demonstration with a T site of myoglobin

1987 ◽  
Vol 246 (2) ◽  
pp. 307-312 ◽  
Author(s):  
M Z Atassi ◽  
M Yoshioka ◽  
M Bean ◽  
G S Bixler
Keyword(s):  
T Cell ◽  
Surface Region ◽  
Protein Chain ◽  
Uniform Size ◽  
Site Specific ◽  
T Cell Clones ◽  
Synthetic Strategy ◽  
Cell Clones ◽  
Discrete Surface ◽  
Lymph Node Cells

Six regions (T sites) of myoglobin (Mb) were found by a comprehensive synthetic strategy to stimulate Mb-primed lymph-node cells. To define precisely the N-terminal boundary of the immunodominant T site (residues 107-120) with site-specific T-cell clones and to determine the effects of peptide size on their stimulation, two sets of peptides were employed. In one set, the peptides were elongated to the left from His-113 by one-residue increments of the Mb sequence. The other set represented an identical stepwise elongation by one-residue increments of the Mb sequence, but which were extended by additional unrelated (‘nonsense’) residues to a uniform size of 14 residues. Examination of the proliferative responses of eight T-cell clones, derived from Mb-primed DBA/2 (H-2d) or SJL (H-2s) mice, revealed a dramatic non-specific size requirement. In every clone, the longer nonsense-extended peptides achieved maximum stimulating activity at a lower optimum peptide dose than its natural-sequence, but shorter, analogue. In addition, slight (one-residue) differences in the N-terminal boundaries among the clones was observed. Thus, the fine specificity of each clone was mapped to the region from residue 111 or 112 to about residue 120 of Mb, which coincides with the site of B-cell recognition and resides in a small discrete surface region of the protein chain.

scholarly journals Site recognition by protein-primed T cells shows a non-specific peptide size requirement beyond the essential residues of the site Demonstration by defining an immunodominant T site in myoglobin

1986 ◽  
Vol 240 (1) ◽  
pp. 139-146 ◽  
Author(s):  
G S Bixler ◽  
M Bean ◽  
M Z Atassi
Keyword(s):  
Surface Region ◽  
Mouse Strains ◽  
Protein Chain ◽  
Uniform Size ◽  
New Approach ◽  
T Cell Stimulation ◽  
Discrete Surface ◽  
Low Responder ◽  
Site Recognition ◽  
Responder Mouse

In previous studies, six T sites within myoglobin (Mb) were localized. To define precisely the boundaries of the T sites, a new approach is introduced and applied here to the T site residing within residues 107-120 of Mb. Two sets of peptides were synthesized. One set represents a stepwise elongation by one-residue increments of the Mb sequence. The other set represents an identical stepwise addition of one-residue increments of the Mb sequence, but which were extended by additional unrelated (nonsense) residues to a uniform size of 14 residues. The longer peptides (nonsense-extended) usually gave higher proliferative responses than did their shorter counterparts having the same Mb region. Thus a minimum peptide size is required for optimal T-cell stimulation. The T site subtends, in three high-responder mouse strains, residues 109-119 or 110-120, depending on strain, and, in three low-responder strains, maps to residues 108-120. Thus, in this case, the T site coincides with the site of B-cell recognition and resides in a small discrete surface region of the protein chain.

scholarly journals Arsonate-specific murine T cell clones. I. Genetic control and antigen specificity

1983 ◽  
Vol 157 (3) ◽  
pp. 987-997 ◽  
Author(s):  
B Hertel-Wulf ◽  
JW Goodman ◽  
CG Fathman ◽  
GK Lewis
Keyword(s):  
T Cell ◽  
Genetic Control ◽  
Cell Interaction ◽  
Antigen Specificity ◽  
T Cell Clones ◽  
Cell Clones ◽  
Homologous Antigen ◽  
Lymph Node Cells ◽  
T Cell Lines ◽  
Antigen Presenting

The antigen-induced proliferative response of lymph node cells (LNC) from mice sensitized to the monofunctional antigen L-tyrosine-p-azobenzenearsonate (ABA-Tyr) was used to monitor genetic control. All strains tested mounted significant responses, but those that were H-2(b) at both the I-A and I-E loci [B10., B6., B10.A(18R), A.BY, and C3H.SW] gave consistently weaker responses than other haplotypes. The F(1) progeny of matings between high and low responder phenotype parents (DBA/2 and B6, respectively) were high responders, establishing the dominance of the responder trait. Proliferative responses of LNC to ABA-Tyr were blocked by the appropriate anti-Ia monoclonal reagents. For example, B10.A(4R) LNCI (I-A(k), I-E(b)) were blocked by anti-I-A(k), whereas B10.A(3R) LNC (I-A(b), I-E(k)) were blocked by anti-I-E(k). Long-term cultures of T cell lines specifically reactive to ABA-Tyr were established from LNC of A/J mice immunized with ABA-Tyr and were cloned by limiting dilution. The proliferative responses to ABA-Tyr of 14 out of 15 clones tested were I-A restricted on the basis of activation by antigen-presenting cells from appropriate recombinant strains and the blocking activity of the monoclonal anti-Ia antibodies. The response of the other clone was I-E restricted. The fine antigen specificity of the clones was studied using structural analogs of the homologous antigen to induce proliferation. The clones could be divided into three types with respect to responsiveness to ABA-histidine (ABA-His). One group responded about equally well to ABA-His and ABA-Tyr. A second set responded less strongly to ABA-His than to ABA-Tyr, while the third showed no response above background to ABA- His. In all instances, the ABA-His-responding clones discriminated exquisitely between the 2-azo and 4-azo histidine isomers, responding only to the 4-azo compound. These T cell clones provide extremely useful tools for studies of T cell specificity, antigen recognition and lymphoid cell interaction systems.

scholarly journals Activation specificity of arsonate-reactive T cell clones. Structural requirements for hapten recognition and comparison with monoclonal antibodies.

1984 ◽  
Vol 159 (2) ◽  
pp. 479-494 ◽  
Author(s):  
A Rao ◽  
S J Faas ◽  
H Cantor
Keyword(s):  
Monoclonal Antibodies ◽  
T Cell ◽  
Antigen Presenting Cells ◽  
Structural Features ◽  
T Cell Clones ◽  
Cell Clones ◽  
Lymph Node Cells ◽  
A Site ◽  
Antigen Presenting

We describe clones of hapten-specific inducer T cells from (BALB/c X A/J)F1 mice that respond to the p-azobenzenearsonate hapten conjugated to carrier proteins or directly conjugated to antigen-presenting cells. Some of the clones are also activated by haptens structurally related to arsonate. All activating analogues are recognized by each clone in association with the same major histocompatibility complex (MHC) protein as is arsonate. Weakly activating and nonactivating analogues are immunogenic in D2.GD amd (BALB/c X A/J)F1 mice, since they can effectively activate primed lymph node cells or long-term hapten-reactive cell lines. Hence the specificities of these clones may reflect their intrinsic recognition of arsonate and its analogues, rather than more efficient presentation of certain analogues than of others by antigen-presenting cells, or differential recognition of associated MHC epitopes by the clones. We compare the activation specificities of the clones with the binding specificities of monoclonal antibodies to arsonate, and discuss structural features of the analogues that may be important for activation and binding. Our results suggest that a site (or subsite) on arsonate-reactive T cell clones may interact directly with hapten, and may be experimentally separable from the site (or subsite) for MHC determinants.

Human Heart–Infiltrating T-Cell Clones From Rheumatic Heart Disease Patients Recognize Both Streptococcal and Cardiac Proteins

Circulation ◽  
1995 ◽  
Vol 92 (3) ◽  
pp. 415-420 ◽  
Author(s):  
L. Guilherme ◽  
E. Cunha-Neto ◽  
V. Coelho ◽  
R. Snitcowsky ◽  
P. M. A. Pomerantzeff ◽  
...  
Keyword(s):  
Heart Disease ◽  
T Cell ◽  
Rheumatic Heart Disease ◽  
Human Heart ◽  
T Cell Clones ◽  
Cell Clones ◽  
Rheumatic Heart

Bacteria-specific CD4+ T-cell clones induce colitis in helicobacter hepaticus-infected T-cell-deficient RAG-2 KO mice

2001 ◽  
Vol 120 (5) ◽  
pp. A519-A520
Author(s):  
Marika C. Kullberg ◽  
Dragana Jankovic ◽  
Patricia Caspar ◽  
Peter L. Gorelick ◽  
Allen Cheever ◽  
...  
Keyword(s):  
T Cell ◽  
Cd4 T Cell ◽  
Helicobacter Hepaticus ◽  
T Cell Clones ◽  
Cell Clones

Development of Lung Eosinophilic Inflammation by the Infusion of IL-5-Producing T Cell Clones

1997 ◽  
Vol 114 (1) ◽  
pp. 10-13 ◽  
Author(s):  
Osamu Kaminuma ◽  
Akio Mori ◽  
Matsunobu Suko ◽  
Hideo Kikkawa ◽  
Kazuaki Naito ◽  
...  
Keyword(s):  
T Cell ◽  
Eosinophilic Inflammation ◽  
T Cell Clones ◽  
Cell Clones

scholarly journals Self-sparing of long-term in vitro-cloned or uncloned cytotoxic T lymphocytes.

1986 ◽  
Vol 164 (3) ◽  
pp. 962-967 ◽  
Author(s):  
M F Luciani ◽  
J F Brunet ◽  
M Suzan ◽  
F Denizot ◽  
P Golstein
Keyword(s):  
T Cell ◽  
T Lymphocytes ◽  
Cytotoxic T Lymphocytes ◽  
Cytotoxic T Cell ◽  
Cell Populations ◽  
Con A ◽  
T Cell Clones ◽  
Cell Clones

At least some long-term in vitro-cultured cytotoxic T cell clones and uncloned cell populations are able, in the presence of Con A, to lyse other cells, to be lysed by other cells, but not to lyse themselves. This as-yet-unexplained result may have implications as to the mechanism of T cell-mediated cytotoxicity.

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