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USMLE Step 1ImmunologyEP 09 of 14

B-cell vs T-cell immunodeficiency: predict the infections

Two babies are both immunodeficient, yet their infections differ. Work out which arm of immunity is lost, antibody or cellular, and the pattern of infection follows.

  • 5:24 video
  • 3 min read
  • 10 sources
  • Published 15 Nov 2026
Video lesson · 5:24 · Watch on YouTubeSeries: Immunology · @medservatory
Chapters (12)
By the end of this lesson

Predict the infection pattern of B-cell, T-cell and combined immunodeficiencies from the arm of immunity lost.

The short version

  1. Antibody loss leaves extracellular, encapsulated bacteria unchecked; T-cell loss leaves viruses, fungi and opportunists unchecked.
  2. In X-linked agammaglobulinaemia a BTK mutation stops B cells maturing at the pre-B stage, so there are almost no B cells and almost no immunoglobulin of any class.
  3. Maternal IgG protects until about six months, so antibody-deficiency infections start as it fades.
  4. Severe combined immunodeficiency loses both arms: it presents in the first few months, and live vaccines can cause the infection they target.
  5. Ask three things: how old, which organisms, and which arm.

Two immunodeficient babies, two different infection patterns

A ten-month-old boy has his third ear infection, and now a pneumonia. He is feeding well and gaining weight. Down the corridor, a two-month-old has thrush that will not clear, and a pneumonia from Pneumocystis.

Both babies are immunodeficient, so why are their infections so different? This lesson on B-cell vs T-cell immunodeficiency shows how to predict the infection pattern from the arm of immunity that is lost.[3][4]

The two arms of immunity: antibody and cellular

  • The antibody arm: B cells become plasma cells, and their antibodies coat microbes so that phagocytes can eat them.[2][3]
  • The cellular arm: cytotoxic T cells kill virus-infected cells, and helper T cells release cytokines that boost the other responses.[1][5]

The rule that follows: lose antibody, and extracellular bacteria win. Lose T cells, and viruses, fungi and opportunists win.[3][4]

Antibody loss: encapsulated bacteria and X-linked agammaglobulinaemia

Without antibody to coat them, encapsulated bacteria slip past phagocytes. The typical organisms are Streptococcus pneumoniae and Haemophilus influenzae, causing sinus, ear, lung and skin infections.[3][4][6]

The classic example is X-linked agammaglobulinaemia (XLA). A mutation in BTK stops B cells maturing at the pre-B stage, so a boy has almost no B cells and almost no immunoglobulin of any class.[3][6]

His T cells are intact, so most viruses are handled. The notorious exceptions are enteroviruses, and the gut parasite Giardia is a recognised risk too.[3][4][6]

T-cell loss: viruses, Candida, Pneumocystis and other opportunists

Without cytotoxic and helper T cells, you see viruses, Candida, and Pneumocystis jirovecii, along with other opportunists.[4][9]

Helper T cells also boost the other responses, so losing them weakens antibody production too.[1][3][4]

Combined loss: severe combined immunodeficiency (SCID)

SCID loses both arms. Babies present in the first few months with Candida, Pneumocystis or severe Escherichia coli infections, and untreated, do not typically survive infancy. The X-linked form is the commonest, nearly half of cases.[3][9]

These babies cannot form memory, so vaccines do not protect them, and live vaccines can cause the very infection they target.[3][9]

Infection pattern by arm of immunity lost
Arm lostTypical infectionsClue
Antibody (B cell), e.g. XLAEncapsulated bacteria: S. pneumoniae, H. influenzae; enteroviruses and GiardiaStarts after about six months, as maternal IgG fades
T cellViruses, Candida, Pneumocystis jirovecii, other opportunistsWeakens antibody production as well
Both (SCID)Candida, Pneumocystis, E. coliFirst few months; live vaccines are dangerous

Back to the two babies: age, organisms, arm

The ten-month-old has bacterial infections after the maternal antibody window, and he is thriving. That is an antibody problem.[3][7]

The two-month-old has thrush and Pneumocystis in the first months. That points to T cells, or a combined defect.[3][4]

  1. How old?The age at which infections began is a clue to the component affected.[4]
  2. Which organisms?Encapsulated bacteria point to antibody; viruses, fungi and Pneumocystis point to T cells.
  3. Which arm?Antibody, T cell, or both, as in SCID.

Practice question

Original · USMLE style
Your turnQB-MS-S1-IMM-004-01

A 9-month-old boy has had four episodes of otitis media and two pneumonias since the age of 7 months. Cultures grew Streptococcus pneumoniae. His growth is normal, and he has had no thrush or diarrhoea. No tonsillar tissue is visible on examination. Serum IgG, IgA and IgM are all markedly decreased. Flow cytometry shows normal numbers of T cells and almost no B cells.

Which of the following best describes the arm of immunity lost, and the infections he is most at risk of?
Pick one option. Your answers stay on this device.

Common questions

What is the difference between B-cell and T-cell immunodeficiency?

B-cell (antibody) deficiency leaves extracellular, encapsulated bacteria such as Streptococcus pneumoniae and Haemophilus influenzae unchecked. T-cell deficiency leaves viruses, fungi, Pneumocystis jirovecii and other opportunists unchecked.

What causes X-linked agammaglobulinaemia?

A mutation in BTK stops B cells maturing at the pre-B stage. The boy has almost no B cells and almost no immunoglobulin of any class.

Why do infections in antibody deficiency start at about six months?

Maternal IgG crosses the placenta and protects the infant. Infections begin as it fades, at about six months.

What is SCID and why are live vaccines a problem?

Severe combined immunodeficiency loses both the antibody and the cellular arm. These babies cannot form memory, so vaccines do not protect them, and live vaccines can cause the very infection they target.

Transcript

Read the full narration, by chapter623 words

0:00The case: two immunodeficient babies, two different infections

A 10-month-old boy has his third ear infection, and now a pneumonia. He is feeding well and gaining weight. Down the corridor, a two-month-old has thrush that will not clear, and a pneumonia from Pneumocystis. Both babies are immunodeficient. So why are their infections so different? Today: predict the infection pattern from the arm of immunity that is lost.

0:25Two arms of immunity: antibody and cellular

Think of two arms. The antibody arm: B cells become plasma cells, and their antibodies coat microbes so that phagocytes can eat them. The cellular arm: cytotoxic T cells kill virus-infected cells, and helper T cells release cytokines that boost the other responses. Lose antibody, and extracellular bacteria win. Lose T cells, and viruses, fungi and opportunists win.

0:55Antibody loss: encapsulated bacteria slip past phagocytes

Without antibody to coat them, encapsulated bacteria slip past phagocytes: Streptococcus pneumoniae and Haemophilus influenzae, causing sinus, ear, lung and skin infections.

1:09X-linked agammaglobulinaemia: BTK, pre-B stage, no immunoglobulin

The classic example is X-linked agammaglobulinaemia. A mutation in BTK stops B cells maturing at the pre-B stage, so a boy has almost no B cells and almost no immunoglobulin of any class. His T cells are intact, so most viruses are handled, though enteroviruses and Giardia are notorious exceptions.

1:34The timing clue: maternal IgG fades at about six months

Timing is the clue: maternal IgG crosses the placenta, so he is protected until about six months, and infections start as it fades.

1:45T-cell loss: viruses, Candida, Pneumocystis, opportunists

Now T-cell loss. Without cytotoxic and helper T cells, you see viruses, Candida, and Pneumocystis jirovecii, along with other opportunists. And because helper T cells boost the other responses, losing them also weakens antibody production.

2:04SCID: both arms lost, the first months, live vaccines

Severe combined immunodeficiency loses both arms. Babies present in the first few months with Candida, Pneumocystis or bad Escherichia coli infections, and untreated, do not typically survive infancy. The X-linked form is commonest, nearly half of cases. These babies cannot form memory, so vaccines do not protect them, and live vaccines can cause the very infection they target.

2:33Back to our babies: age, organisms, arm

Back to our babies. The 10-month-old: bacterial infections after the maternal antibody window, and he is thriving. That is an antibody problem. The two-month-old: thrush and Pneumocystis in the first months. That points to T cells, or a combined defect. Ask three things: how old, which organisms, and which arm.

2:59Your turn: a practice question

Your turn. A nine-month-old boy has had four ear infections and two pneumonias since the age of seven months, and cultures grew Streptococcus pneumoniae. His growth is normal, with no thrush or diarrhoea, and no tonsillar tissue is visible. Serum IgG, IgA and IgM are all markedly decreased. Flow cytometry shows normal T cells and almost no B cells. Which of the following best describes the arm of immunity lost, and the infections he is most at risk of? A, T-cell function; Pneumocystis, Candida and cytomegalovirus. B, both T and B cells; opportunistic infections from early infancy. C, phagocyte oxidative killing; staphylococci and Aspergillus. D, terminal complement; recurrent Neisseria infection. E, antibody production; encapsulated bacteria, enteroviruses and Giardia. Pause here and decide.

4:06The options, one at a time

A is out: T-cell loss brings viruses, Candida and Pneumocystis, and his T cells are normal. B is out: a combined defect presents in the first months with opportunists, and his T cells are normal. C is out: failed oxidative killing gives staphylococcal and Aspergillus infections, with normal immunoglobulins. D is out: terminal complement loss gives recurrent Neisseria, and does not lower immunoglobulins.

4:36The answer is E

So the answer is E. Every immunoglobulin class is low with almost no B cells, he fell ill after the maternal antibody faded, and antibody loss leaves him open to encapsulated bacteria.

4:53Recap pocket card and the next lesson

Three things to keep. One: antibody loss means encapsulated bacteria, starting after about six months. Two: T-cell loss means viruses, fungi and Pneumocystis. Three: combined loss, SCID, shows up in the first months and needs treatment early. Next, hyper-IgM syndrome, where antibody production fails for a reason in the T cell.

Sources

Numbers in the text, e.g. [1], point here
  1. OpenStax. Anatomy and Physiology 2e, 21.3 The Adaptive Immune Response: T Lymphocytes and Their Functional Types. openstax.org/books/anatomy-and-physiology-2e/pages/21-3-the-adaptive-immune-response-t-lymphocytes-and-their-functional-types
  2. OpenStax. Anatomy and Physiology 2e, 21.4 The Adaptive Immune Response: B Lymphocytes and Antibodies. openstax.org/books/anatomy-and-physiology-2e/pages/21-4-the-adaptive-immune-response-b-lymphocytes-and-antibodies
  3. OpenStax. Microbiology, 19.4 Immunodeficiency. openstax.org/books/microbiology/pages/19-4-immunodeficiency
  4. MSD Manual Professional Version. Overview of Immunodeficiency Disorders. msdmanuals.com/professional/immunology-allergic-disorders/immunodeficiency-disorders/overview-of-immunodeficiency-disorders
  5. MSD Manual Professional Version. Overview of the Immune System. msdmanuals.com/professional/immunology-allergic-disorders/biology-of-the-immune-system/overview-of-the-immune-system
  6. Agammaglobulinemia: from X-linked to autosomal forms. Europe PMC, PMC8269404. europepmc.org/article/PMC/PMC8269404
  7. Novel BTK mutation and late diagnosis of X-linked agammaglobulinaemia. Europe PMC, PMC10693464. europepmc.org/article/PMC/PMC10693464
  8. Inborn errors of immunity, review. Europe PMC, PMC11714877. europepmc.org/article/PMC/PMC11714877
  9. How I Treat infections and inborn errors of immunity. Europe PMC, PMC12829740. europepmc.org/article/PMC/PMC12829740
  10. Staudacher O, von Bernuth H. Chronic granulomatous disease: S. aureus and Aspergillus infections. Europe PMC, PMC11239527. europepmc.org/article/PMC/PMC11239527

The practice question is original and its patient is synthetic. Every fact is checked against the sources above in independent accuracy reviews. Always follow your local guidelines and your own laboratory’s ranges.

Image credits. Illustrations: Servier Medical Art (smart.servier.com), CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/), adapted (recoloured, outlined, cropped): Candida albicans, herpes virus. Cell icons by Servier via Bioicons (bioicons.com), CC BY 3.0 (https://creativecommons.org/licenses/by/3.0/), adapted (recoloured, outlined): b-lymphocyte, t-lymphocyte, antibody, neutrophil-granulocyte. plasma_cell icon by El-Jayawant via Bioicons, CC BY 4.0. Lymph node: NIAID NIH BIOART Source (bioart.niaid.nih.gov/bioart/304), public domain. Icons: Health Icons (healthicons.org), CC0: baby (two ages), ear, pneumonia, vaccine syringe. The two-arms diagram, bacteria and capsule sketches, B-cell development strip, immunoglobulin bars, maternal-IgG timeline (schematic, not patient data), pattern table, cards and all handwriting are drawn in code (original). No AI-generated teaching images.

Corrections. None so far. Spotted an error? Email info@medservatory.com with the lesson code MS-S1-IMM-004.

For exam study only, not medical advice. Read the medical disclaimer.

In this series

Playlist on YouTube
← Previous · EP 08Hypersensitivity types I to IV: the four effectors
  1. EP 01MHC I vs MHC II: how antigen presentation works5:03
  2. EP 02T-cell activation: the two-signal model4:58
  3. EP 03Th1, Th2, Th17 and Treg: helper T-cell subsets5:13
  4. EP 04Antibody isotypes and class switching5:13
  5. EP 05Central vs peripheral tolerance: how lymphocytes learn self-tolerance5:26
  6. EP 06Complement system explained: three pathways, one ending5:24
  7. EP 07Complement deficiencies: C1q, C3, C5–C9 and C1 inhibitor5:15
  8. EP 08Hypersensitivity types I to IV: the four effectors5:20
  9. EP 09B-cell vs T-cell immunodeficiency: predict the infections5:24
  10. EP 10Hyper IgM syndrome: CD40 ligand and class switching5:19
  11. EP 11Chronic granulomatous disease: NADPH oxidase and the respiratory burst5:20
  12. EP 12Leukocyte adhesion deficiency: CD18 and neutrophil extravasation5:01
  13. EP 13Transplant rejection explained: hyperacute, acute, chronic and GVHD5:51
  14. EP 14Vaccine types explained: live, inactivated, conjugate and mRNA5:41