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Question #45464
The Question
A patient exhibits a severely compromised cell-mediated immune response. Laboratory analysis reveals abnormally elevated levels of circulating thymosins but a complete absence of mature T-lymphocytes. Assuming the defect lies in the hormonal signaling pathway, which of the following statements correctly identifies the nature of the defect and its immediate biochemical consequence?
Options
- A.
A mutation in the intracellular receptor for thymosin prevents the hormone-receptor complex from interacting with the genome.
- B.
A structural defect in the membrane-bound receptor prevents thymosin binding, leading to a failure in generating secondary messengers like cAMP.
- C.
Degeneration of the thymus gland leads to a lack of primary messengers, causing a compensatory increase in intracellular Ca2+.
- D.
A defect in the lipid bilayer prevents the entry of thymosin into the target cell, halting the secondary messenger cascade.
Check Your Answer
Correct Answer
Step-by-Step Solution
Explanation
How the Examiner Thinks
Comparative_Analysis
Sharpen your ability to evaluate multiple scenarios and distinguish between competing potential answers.
Concepts Behind This Question
Thymosin Specificity|Secondary Messenger Cascade|Hormone Receptors Location
Why This Question Is Tricky
Common Mistakes
Conceptual Pivot: The question tests two overlapping NCERT concepts: the chemical nature of Thymosin (peptide hormone) and the mechanism of hormone action (membrane-bound receptors vs. intracellular receptors).
The trap lies in distinguishing between hormone deficiency (low production) and hormone resistance (receptor mutation).
Students often incorrectly assume peptide hormones must enter the cell to function (Option D) or confuse them with steroid mechanisms (Option A).
Quick Facts About This Question
Question Information
| Subject | Biology |
| Chapter | Chemical Coordination and Integration - Class 11 |
| Concept | Thymosin Specificity |
| Difficulty | 8 |
| Cognitive Load | 5 |
| Target Solve Time | 120 sec |
| Access | Free |