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測驗


本頁翻譯進度

燈號說明

審定:謝怡玲
審定簡介:
課程中譯計劃審定老師

翻譯:陳致宇(簡介並寄信)
編輯:朱學(簡介並寄信)

下面是期末考試題的範本。你也可以直接下載考試的試題。
(英文PDF)


期末測驗

請回答下列所有的問題。請務必簡短並切中要點。

問題 1

a) 在缺少CD40L的老鼠和X性聯遺傳過度IgM症候群的男孩身上,可以發現細胞免疫缺乏的現象。病人很容易產生肺囊孢仔蟲肺炎。為什麼缺少CD40L會導致CMI的缺陷(5分)?

b) 以圖示方式解釋(畫出你所知道到相關的路徑)為何IKK-(IB激脢,也稱做NEMO)低型態同型合子突變可能產生過度IgM症候群(10分)?

c) AID出生就發生突變的小孩會產生產生類過度IgM症候群並且無法產生高結合力的抗體。請回答什麼是AID在自體突變中可能扮演的基本功能作用(10分)?

問題 2

超抗原可以和許多TCR上的V區域結合並同時也和抗原呈現細胞上的第二類MHC分子有關(請參考附圖)。在所有的CD4 T細胞中(這些細胞有同一小組的V範圍),其中有5-20%其TCR上的第二類MHC分子可以和典型的超抗原交互連結。超抗原和"正常的"抗原不同,而且它們也不和第二類凹槽結合。它們會和第二類分子的結構決定部位和特殊V蛋白的架構決定部位結合,而且可以不必共同刺激物。

a) 由金黃色葡萄球菌TSST1毒素引起的毒性休克症候群中,TSST1已經被證實是種會產生高燒,休克以及廣泛性紅斑的超抗原。它可能會致命。藉由以上的資訊,你認為(用一兩句話描述)造成這個症候群的致病機轉主要原因為何(5分)?

b) 一種會和老鼠TCR中V4和V11部位結合的超抗原被基因轉植到老鼠身上。經過基因轉植的老鼠可以存活。有人給你會和所有20種老鼠V蛋白家族反應的單株抗體(從V1到V20)。你預期在基因轉植鼠和未經轉植鼠的免疫系統,會不會觀察到有任何差異?不要用超過一句來解釋(5分)。

c) 簡單解釋HLA-DM的功能(5分)。

Q問題 3

粒酵素B的受質專一性是什麼(5分)?到底什麼是胱冬?酵素?(5分)。陽離子相關的mannose-6-phosphate受體(CI-M6PR)是一種可以做為細胞表面內噬作用的受體,而在腫瘤細胞,這個蛋白的基因常常會被刪除。它的功能是腫瘤抑制,而失去兩個基因座會造成腫瘤生長。會什麼你認為失去CI-M6PR會造成腫瘤生成?(回答請勿超過兩句)(5分)。

問題 4

以條列式列出三個可以使腫瘤特定蛋白被宿主T細胞辨識為腫瘤抗原的方法(10分)。.

問題 5

描述環孢素A如何干擾細胞激素的轉錄作用(10分)。

問題 6

a) 直接接種由細菌所獲得的質體DNA會誘導免疫反應。假設這個質體DNA不含內毒素,提出理由說明你認為"危險"訊息是源自細菌的DNA或是質體(5分)。

b) 信號一和信號二如何在細胞質和細胞核互相配合,在T細胞活化時誘導IL-2轉錄作用?請力求簡短(5分)。

問題 7

AIRE在哪裡表現,而其功能為何?(5分)?你為什麼認為AIRE突變的病人會發生反覆性的黏液皮層的念珠菌感染(5分)?




Below is a sample final exam from the course. You may also download a copy of the exam.

Final Examination

Please answer all questions. Be brief and to the point.

Question 1

a) In mice that lack CD40L, as well as in boys with the X-linked hyper-IgM syndrome, a deficiency in cell mediated immunity is observed. Pneumocystis carinii pneumonia is a common presentation in patients. Why does the absence of the CD40L lead to a defect in CMI (5 points)?

b) Explain with the aid of a diagram (showing what you know of the pathway involved) why a homozygous hypomorphic mutation in IKK- (I B kinase, also known as NEMO) might contribute to a hyper-IgM like syndrome (10 points).

c) Children born with mutant AID develop a hyper-IgM like syndrome and fail to generate high affinity antibodies. What is the mechanistic basis for AID's presumed role in somatic mutation (10 points) ?

Question 2

Superantigens can bind to a large number of V regions on TCRs and simultaneously also associate with MHC class II molecules on APCs (see figure). A typical superantigen may crosslink MHC class II molecules to TCRs on as many as 5-20% of all CD4 T cells (which all share a subset of V domains). Superantigens are distinct from "normal" antigens and they do not bind to the class II groove. They bind to structural determinants on class II molecules and framework determinants on specific V proteins, and can bypass the need for costimulation.

a) In the Toxic shock syndrome caused by the TSST1 toxin from S.aureus, TSST1 has been demonstrated to be a superantigen that causes high fever, shock, and a diffuse erythematous rash. It can be life-threatening. Given the above information, what do you think (in one or two sentences) is the pathogenic basis of this syndrome? (5 points)

b) A superantigen that binds to V 4 and V 11 containing murine TCRs was expressed transgenically in mice. Transgenic mice are viable. You are given monoclonal antibodies to all 20 murine V family proteins (V 1 to V 20). Do you expect to see any differences in the immune system between transgenic and non-transgenic mice? Explain in no more than one sentence (5 points).

c) Explain briefly the function of HLA-DM (5 points).

Question 3

What is granzyme B's substrate specificity (5 points)? What exactly are caspases? (5 points). The cation-independent mannose-6-phosphate receptor (CI-M6PR) is a protein that can function as a cell surface endocytic receptor and the gene for this protein is frequently deleted in tumors. It is a tumor suppressor - loss of both alleles favors tumor progression. Why do you think loss of CI-M6PR favors tumorigenesis? (No more than two sentences please) (5 points).

Question 4

Describe in a point-by-point manner three ways in which certain proteins in tumors might be recognized as tumor antigens by host T cells (10 points).

Question 5

Describe how cyclosporin A interferes with cytokine gene transcription (10 points).

Question 6

a) Direct immunization with plasmid DNA of bacterial origin induces immune responses. Assuming that the plasmid DNA is endotoxin-free, mention how you think "danger" is signaled by DNA of bacterial or plasmid origin (5 points).

b) How do signal one and signal two cooperate in the cytosol and nucleus to induce IL-2 transcription during T cell activation? Please be brief (5 points).

Question 7

Where is AIRE expressed and what is it's presumed function? (5 points)? Why do you think patients with AIRE mutations develop recurrent mucocutaneous candidiasis (5 points)?




 
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