Abbas: Cellular and Molecular Immunology, 7 th Edition Activation of T Lymphocytes Test an! Multiple Choice
1. All of the followin following g protein-prote protein-protein in interaction interactionss are involved involved in activation activation of naive helper T cells by antigen-presenting cells (APCs) EXCEPT binding EXCEPT binding of A. Peptide-!"C co#ple$es on the APC to the the TC% on the T cell &. C' on the T cell to nonpoly#orphic regions of class !"C #olec*les #olec*les on the APC APC C. ntegrins ntegrins on the T cell with with adhesion ligands ligands on the APC APC '. &+-, on the APC APC with C', C', on the T cell E. C'/ on the T cell cell with with C' on the APC A0 E. C'/ is not e$pressed on naive T cells and is only *p-reg*lated s*bse2*ent to activation by an antigen-presenting cell (APC). n the naive helper T cell3 the TC% binds to the !"C-peptide co#ple$ whereas the C' coreceptor engages a conserved region on the !"C #olec*le. ntegrins on the T cell interact with adhesion ligands on the APC. This region of binding between the T cell and the APC is 4nown as the i##*nologic synapse and also incl*des costi#*latory interactions3 s*ch as C', on the T cell binding to &+ on the APC. ,. 5hich one of the the following following state#ents state#ents abo*t abo*t !"C-TC% !"C-TC% interacti interactions ons is 06T tr*e7 tr*e7 A. Antigen receptors on T cells bind to !"C #olec*les for only brief periods of ti#e. &. The affinity affinity of #ost TC%s for peptide-!"C peptide-!"C co#ple$es co#ple$es is si#ilar to the affinity affinity of antibodies for their antigens. C. 6nly 18 or less of the !"C #olec*les #olec*les on any antigen-pre antigen-presenti senting ng cell (APC) display display a peptide recogni9ed by a partic*lar T cell. '. T cells cells *s*ally *s*ally re2*ir re2*iree #*ltip #*ltiple le engage# engage#ent entss with with an APC before before a thresh threshold old of activation is reached. E. A s*bthreshold n*#ber of !"C-TC% interactions can lead to T cell inactivation. A0 &. n general3 the TC% binds to peptide-!"C co#ple$es with lower affinity than antigen-antibody interactions. This relatively low-affinity interaction occ*rs briefly: th*s3 a T cell #ay need #*ltiple engage#ents with the antigen-presenting cell (APC) before a threshold of activation occ*rs. f this threshold is not reached3 the T cell #ay enter into an inactive state 4nown as anergy. 6n any given APC3 less than 18 of the !"C #olec*les display the sa#e peptide.
Matching "uestions #$%&
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Test &an4
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?or each of the descriptions in 2*estions =-13 choose the T cell signaling #olec*le that best #atches it fro# the list below (A-6). A. C'= &. /c4 C. @ap-+ '. /AT E. %as ?. P/Cγ . PP, ". PP= . P= B. 'A . Calcine*rin /. 0?AT !. B*n 0. ?os 6. 0?-κ & =. This #olec*le beco#es an active transcription factor on dephosphorylation. A0 /. 0?AT is a transcription factor re2*ired by T cells for the e$pression of interle*4in (/)-,3 /-3 t*#or necrosis factor (T0?)3 and other cyto4ine genes. 0?AT is present in an inactive3 phosphorylated for# in the cytosol of resting T cells. 6n dephosphorylation by calcine*rin3 a n*clear locali9ation se2*ence is *ncovered that per#its 0?AT to translocate to the n*cle*s. 6nce in the n*cle*s3 0?AT ind*ces transcription of these genes.
. This protein is a well-characteri9ed proto-oncogene prod*ct that on #*tation to a constit*tively active for# has been associated with #*ltiple neoplas#s. A0 E. Ras was one of the first proto-oncogenes characteri9ed. 0or#al ras is involved in TC% signaling pathways. 6n #*tation to a constit*tively active state3 ras pro#otes the s*rvival and proliferation of #alignant cells.
<. &inding of this #olec*le to B*n is needed for transcriptional activation of the /-, gene. A0 0. ?os co#bines with phosphorylated B*n to for# activation protein-1 (AP-1). AP1 is the na#e for a fa#ily of '0A-binding factors co#posed of di#ers of two different proteins. Transcription of fos is enhanced by the Er4 pathway3 whereas phosphorylation of pree$isting B*n is ind*ced thro*gh the Dav%ac pathway. AP-1 physically associates with other transcription factors in the n*cle*s3 and together they activate transcription of cyto4ine genes essential for T cell activation.
F. This is a transcription factor that e$ists in the phosphorylated for# within the n*cle*s.
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Test &an4
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A0 !. 6n phosphorylation3 c-B*n translocates to the n*cle*s and binds to ?os to for# AP-1.
+. ##*nos*ppressive therapy with the dr*gs cyclosporine and ?<F inhibits T cell activation by bloc4ing the protein phosphatase activity of this #olec*le. A0 . Calcine*rin is responsible for the dephosphorylation of 0?AT3 which is an essential transcription factor for the activation of T and & cells. The i##*nos*ppressive dr*gs cyclosporine and ?<F f*nction by inhibiting calcine*rin. These dr*gs are co##only *sed to prevent transplant reGection.
. This #olec*le binds to a receptor on the endoplas#ic retic*l*# and sti#*lates release of calci*# into the cytosol. A0 . P= is generated fro# the cleavage of PP, in the #e#brane to 'A and P= by the en9y#e P/Cγ 3 and it sti#*lates release of calci*# into the cytosol.
>. This #olec*le has the sa#e downstrea# effect as addition of the dr*g phorbol #yristate acetate (P!A) to T cells. A0 B. &oth 'A and phar#acologic agents s*ch as phorbol #yristate acetate (P!A) activate protein 4inase C (PC). PC has #any s*bstrates and is a potent activator of #any transcription factors in T cells.
1. This #olec*le is a transcription factor involved in the e$pression of several T cell activation genes activated when its bo*nd inhibitor is phosphorylated. A0 6. 0?-κ & is present in the cytoplas# and is bo*nd to an inhibitor called - κ &. 6n sti#*lation with antigen3 -κ & beco#es phosphorylated3 dissociates fro# 0?-κ &3 and is degraded by the *bi2*itin-proteoso#al pathway. 0?-κ & then translocates to the n*cle*s3 where it participates in transcriptional activation of several genes.
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