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Primary Immunodeficiencies

Humoral immunity deficiencies Cellular immunity deficiencies Combined humoral and cellular immunity deficiencies Phagocytic cell defects Complement deficiencies Primary immunodeficiency references

Key Points

Immunodeficiency Disorders

Overview of Immunodeficiency Disorders

Approach to the Patient With Suspected Immunodeficiency

Ataxia-Telangiectasia

Chédiak-Higashi Syndrome

Chronic Granulomatous Disease (CGD)

Chronic Mucocutaneous Candidiasis

Common Variable Immunodeficiency (CVID)

DiGeorge Syndrome

Hyper-IgE Syndrome

Hyper-IgM Syndrome

Selective IgA Deficiency

Leukocyte Adhesion Deficiency

Selective Antibody Deficiency With Normal Immunoglobulins (SADNI)

Severe Combined Immunodeficiency (SCID)

Transient Hypogammaglobulinemia of Infancy

Wiskott-Aldrich Syndrome

X-linked Agammaglobulinemia

X-linked Lymphoproliferative Syndrome

ZAP-70 Deficiency

Of the four possible abnormal lymphocyte phenotypes in patients with severe combined immunodeficiency (SCID), which of the following is the most common?

T+ B- NK-
T- B- NK-
T- B+ NK-
T- B+ NK+

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By

James Fernandez

, MD, PhD, Cleveland Clinic Lerner College of Medicine at Case Western Reserve University

Last full review/revision Dec 2019| Content last modified Dec 2019

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Topic Resources

Humoral Immunity Deficiencies

Cellular Immunity Deficiencies

Combined Humoral and Cellular Immunity Deficiencies

Phagocytic Cell Defects

Complement Deficiencies

Causes of Secondary Immunodeficiency

Some Drugs That Cause Immunosuppression

Immunodeficiency disorders are associated with or predispose patients to various complications, including infections, autoimmune disorders, and lymphomas and other cancers. Primary immunodeficiencies are genetically determined and can be hereditary; secondary immunodeficiencies are acquired and much more common.

Evaluation of immunodeficiency includes history, physical examination, and immune function testing. Testing varies based on the following:

Whether a primary or secondary immunodeficiency is suspected
For primary immunodeficiency, which component of the immune system is thought to be deficient

These disorders are genetically determined; they may occur alone or as part of a syndrome. In 2017, the International Union of Immunological Sciences reported that 354 inborn errors of immunity and 344 genes have been linked to primary immunodeficiency disorders (1).The molecular basis for about 80% is known.

Primary immunodeficiencies typically manifest during infancy and childhood as abnormally frequent (recurrent) or unusual infections. About 70% of patients are < 20 years at onset; because transmission is often X-linked, 60% are male. Overall incidence of symptomatic disease is about 1/280 people.

Primary immunodeficiencies are classified by the main component of the immune system that is deficient, absent, or defective:

As more molecular defects are defined, classifying immunodeficiencies by their molecular defects will become more appropriate (2).

Primary immunodeficiency syndromes are genetically determined immunodeficiencies with immune and nonimmune defects. Nonimmune manifestations are often more easily recognized than those of the immunodeficiency. Examples are ataxia-telangiectasia, cartilage-hair hypoplasia, DiGeorge syndrome, hyper-IgE syndrome, and Wiskott-Aldrich syndrome. Despite the presence of immunodeficiencies, some patients also develop autoimmune disorders.

Immunodeficiency typically manifests as recurrent infections. The age at which recurrent infections began provides a clue as to which component of the immune system is affected. Other characteristic findings tentatively suggest a clinical diagnosis (see Characteristic Clinical Findings in Some Primary Immunodeficiency Disorders). However, tests are needed to confirm a diagnosis of immunodeficiency (see Initial and Additional Laboratory Tests for Immunodeficiency). If clinical findings or initial tests suggest a specific disorder of immune cell or complement function, additional tests are indicated (see Specific and Advanced Laboratory Tests for Immunodeficiency).

Treatment and prognosis of primary immunodeficiency disorders depend on the specific disorder (3).

Humoral immunity deficiencies (B-cell defects) that cause antibody deficiencies account for 50 to 60% of primary immunodeficiencies (see table Humoral Immunity Deficiencies). Serum antibody titers decrease, predisposing to bacterial infections.

The most common B-cell disorder is

Selective IgA deficiency

For diagnostic evaluation of humoral immunity deficiencies, see Approach to the Patient With Suspected Immunodeficiency and table Specific and Advanced Laboratory Tests for Immunodeficiency.

Humoral Immunity Deficiencies

Disorder	Inheritance	Genes Affected	Clinical Findings
Common variable immunodeficiency	Variable	BAFFR, CTLA4, ICOS, NKFKB2, PIK3CD, STAT3, TACI	Recurrent sinopulmonary infections, autoimmune disorders (eg, immune thrombocytopenia, autoimmune hemolytic anemia), malabsorption, giardiasis, granulomatous interstitial lung disease, nodular lymphoid hyperplasia of the GI tract, bronchiectasis, lymphocytic interstitial pneumonia, splenomegaly; in 10%, gastric carcinoma and lymphoma Usually diagnosed in patients aged 20–40 years
Hyper-IgM syndrome with AID or UNG deficiencies	Autosomal recessive	AID, UNG	Similar to X-linked hyper-IgM syndrome but with lymphoid hyperplasia No leukopenia
Hyper-IgM syndrome with CD40 deficiency	Autosomal recessive	CD40	Similar to X-linked hyper-IgM syndrome Lymphoid hypoplasia, neutropenia
Hyper-IgM syndrome with CD40 ligand deficiency	X-linked	CD40 ligand (CD40L)	Similar to X-linked agammaglobulinemia (eg, recurrent pyogenic bacterial sinopulmonary infections) but greater frequency of Pneumocystis jirovecii pneumonia, cryptosporidiosis, severe neutropenia, and lymphoid hypoplasia
Selective antibody deficiency with normal immunoglobulins	Unknown	—	Recurrent sinopulmonary infections Sometimes atopic manifestations (eg, atopic dermatitis, asthma, chronic rhinitis) Can occur in mild, moderate, severe, and memory phenotypes
Selective IgA deficiency	Unknown	In some cases, TACI	Most often asymptomatic Recurrent sinopulmonary infections, diarrhea, allergies (including anaphylactic transfusion reactions [rare]), autoimmune disorders (eg, celiac disease, inflammatory bowel disease, SLE, chronic active hepatitis)
Transient hypogammaglobulinemia of infancy	Unknown	—	Usually asymptomatic Sometimes recurrent sinopulmonary or GI infections, candidiasis, meningitis
X-linked agammaglobulinemia	X-linked	BTK	Recurrent sinopulmonary and skin infections during infancy, transient neutropenia, lymphoid hypoplasia Persistent CNS infections resulting from live-attenuated oral polio vaccine, echoviruses, or coxsackieviruses Increased risk of infectious arthritis, bronchiectasis, and certain cancers
AID= activation-dependent (induced) cytidine deaminase; BAFFR = B-cell activating factor receptor; BTK = Bruton tyrosine kinase; C = complement; CAML = calcium-modulator and cyclophilin ligand; CD = clusters of differentiation; CNS = central nervous system; CTLA4 = cytotoxic T-lymphocyte-associated protein 4; GI = gastrointestinal; ICOS = inducible T-cell co-stimulator; NKFKB2 = nuclear factor kappa B subunit 2PIK3CD = phosphatidyl 3-kinase catalytic subunit delta; SLE = systemic lupus erythematosus; STAT3 = signal transducer and activator of transcription 3; TACI = transmembrane activator and CAML interactor; UNG = uracil DNA glycosylase.

Cellular immunity deficiencies (T-cell defects) account for about 5 to 10% of primary immunodeficiencies and predispose to infection by viruses, Pneumocystis jirovecii, fungi, other opportunistic organisms, and many common pathogens (see table Cellular Immunity Deficiencies). T-cell disorders also cause Ig deficiencies because the B- and T-cell immune systems are interdependent.

The most common T-cell disorders are

Primary natural killer cell defects, which are very rare, may predispose to viral infections and tumors. Secondary natural killer cell defects can occur in patients who have various other primary or secondary immunodeficiencies.

For diagnostic evaluation of cellular immunity deficiencies, see tables Initial and Additional Laboratory Tests for Immunodeficiency and Specific and Advanced Laboratory Tests for Immunodeficiency.

Cellular Immunity Deficiencies

Disorder	Inheritance	Gene Affected	Clinical Findings
Chronic mucocutaneous candidiasis	Autosomal dominant or recessive	STAT1 (dominant) AIRE (recessive)	Persistent or recurrent candidal infections, onychomycosis, autosomal recessive autoimmune polyendocrinopathy–candidosis-ectodermal dystrophy (with hypoparathyroidism and adrenal insufficiency)
DiGeorge syndrome	Autosomal	Genes at chromosomal region 22q11.2 Genes at chromosome 10p13	Characteristic facial appearance with low-set ears, a congenital heart disorder (eg, aortic arch abnormalities), thymic hypoplasia or aplasia, hypoparathyroidism with hypocalcemic tetany, recurrent infections, developmental delay
X-linked lymphoproliferative syndrome	X-linked	SH2D1A (type 1) XIAP (type 2)	Asymptomatic until onset of Epstein-Barr virus infection, then fulminant or fatal infectious mononucleosis with liver failure, B-cell lymphomas, splenomegaly, aplastic anemia
Zeta-associated protein 70 (ZAP-70) deficiency	Autosomal recessive	ZAP-70	Common and opportunistic infections No CD8 cells
AIRE = autoimmune regulator; CD = clusters of differentiation; SH2D1A = SH2 domain containing 1A; STAT = signal transducer and activator of transcription; XIAP = X-linked inhibitor of apoptosis.

Combined humoral and cellular immunity deficiencies (B- and T-cell defects) account for about 20% of primary immunodeficiencies (see table Combined Humoral and Cellular Immunity Deficiencies).

The most important form is

Severe combined immunodeficiency (SCID)

In some forms of combined immunodeficiency (eg, purine nucleoside phosphorylase deficiency), Ig levels are normal or elevated, but because of inadequate T-cell function, antibody formation is impaired.

For diagnostic evaluation of combined humoral and cellular immunodeficiencies, see table Specific and Advanced Laboratory Tests for Immunodeficiency.

Combined Humoral and Cellular Immunity Deficiencies

Disorder	Inheritance	Gene Affected	Clinical Findings
Ataxia-telangiectasia	Autosomal recessive	ATM	Ataxia, telangiectasias, recurrent sinopulmonary infections, endocrine abnormalities (eg, gonadal dysgenesis, testicular atrophy, diabetes mellitus), increased risk of cancer
Cartilage-hair hypoplasia	Autosomal recessive	RMRP	Short-limbed dwarfism, common and opportunistic infections
Combined immunodeficiency with inadequate but not absent T-cell function and normal or elevated immunoglobulins	Autosomal recessive or X-linked	NEMO	Common and opportunistic infections, lymphopenia, lymphadenopathy, hepatosplenomegaly, skin lesions resembling those of Langerhans cell histiocytosis in some patients
Hyper-IgE syndrome	Autosomal dominant or recessive	STAT3 (dominant) TYK2, DOCK8 (recessive)	Sinopulmonary infections; staphylococcal abscesses of skin, lungs, joints, and viscera; pulmonary pneumatoceles; pruritic dermatitis; coarse facial features; delayed shedding of baby teeth; osteopenia; recurrent fractures; tissue and blood eosinophilia
MHC antigen deficiencies	Autosomal recessive	Various including, RFX: RFXANK, RFX5, and RFXAP	Common and opportunistic infections
Severe combined immunodeficiency	Autosomal recessive or X-linked	JAK3, PTPRC (CD45), RAG1, RAG2 (autosomal recessive) IL-2RG(X-linked)	Oral candidiasis, Pneumocystis jirovecii pneumonia, diarrhea before 6 months, failure to thrive, graft vs host disease, absent thymic shadow, lymphopenia, bone abnormalities (in ADA deficiency), exfoliative dermatitis as part of Omenn syndrome*
Wiskott-Aldrich syndrome	X-linked recessive	WASP	Typically, pyogenic and opportunistic infections, eczema, thrombocytopenia Possibly gastrointestinal bleeding (eg, bloody diarrhea), recurrent respiratory infections, cancer (in 10% of patients > 10 years), varicella-zoster virus infection, herpesvirus infection
* Omenn syndrome is an autosomal recessive form of severe SCID causing erythroderma, desquamation, alopecia, chronic diarrhea, failure to thrive, lymphadenopathy, eosinophilia, hepatosplenomegaly, and elevated serum IgE levels.
ADA = adenosine deaminase; ATM = ataxia telangiectasia–mutated; DOCK = dedicator of cytokinesis; IL-2RG = IL-2 receptor gamma; JAK = Janus kinase; MHC = major histocompatibility complex; NEMO = nuclear factor–kappa-B essential modulator; PTPRC = protein tyrosine phosphatase, receptor type, C; RAG = recombination activating gene; RFX = regulatory factor X; RFXANK= RFX containing ankyrin repeats; RFXAP = RFX-associated protein; RMRP = ribonuclease mitochondrial RNA-processing; SCID = severe combined immunodeficiency; STAT = signal transducer and activator of transcription; TYK = tyrosine kinase; WASP = Wiskott-Aldrich syndrome protein.

Phagocytic cell defects account for 10 to 15% of primary immunodeficiencies; the ability of phagocytic cells (eg, monocytes, macrophages, granulocytes such as neutrophils and eosinophils) to kill pathogens is impaired (see table Phagocytic Cell Defects). Cutaneous staphylococcal and gram-negative infections are characteristic.

The most common (although still rare) phagocytic cell defects are

Chronic granulomatous disease
Leukocyte adhesion deficiency (types 1 and 2)
Cyclic neutropenia
Chédiak-Higashi syndrome

For diagnostic evaluation of phagocytic cell defects, see tables Initial and Additional Laboratory Tests for Immunodeficiency and Specific and Advanced Laboratory Tests for Immunodeficiency.

Phagocytic Cell Defects

Disorder	Inheritance	Genes Affected	Clinical Findings
Chédiak-Higashi syndrome	Autosomal recessive	LYST (CHS1)	Oculocutaneous albinism, recurrent infections, fever, jaundice, hepatosplenomegaly, lymphadenopathy, neuropathy, pancytopenia, bleeding diathesis
Chronic granulomatous disease	X-linked or autosomal recessive	gp91phox (CYBB; X-linked) p22phox, p47phox, p67phox (autosomal recessive)	Granulomatous lesions in the lungs, liver, lymph nodes, and gastrointestinal and genitourinary tracts (causing obstruction); lymphadenitis; hepatosplenomegaly; skin, lymph node, lung, liver, and perianal abscesses; osteomyelitis; pneumonia; staphylococcal, gram-negative, and aspergillus infections
Leukocyte adhesion deficiency	Autosomal recessive	ITGB2 gene, encoding CD18 of beta-2 integrins (type 1) GDP-fucose transporter gene (type 2)	Soft-tissue infections, periodontitis, poor wound healing, delayed umbilical cord detachment, leukocytosis, no formation of pus Developmental delay (type 2)
Mendelian susceptibility to mycobacterial disease (MSMD)	Autosomal dominant or recessive	Defects in genes encoding the IFN-gamma receptor, IL-12, or the IL-12 receptor	Mycobacterial infections Varying clinical severity based on genetic defect
Cyclic neutropenia	Autosomal dominant	ELA2	Pyogenic bacterial infections during recurrent episodes of neutropenia (eg, every 14 to 35 days)
CD = clusters of differentiation; CHS = Chédiak-Higashi syndrome; CYBB = cytochrome b-245, beta polypeptide; ELA = elastase; GDP = glucose diphosphate; gp = glycoprotein; IFN = interferon; IL = interleukin; ITGB2 = integrin beta-2; LYST = lysosomal transporter.

Complement deficiencies are rare (≤ 2%); they include isolated deficiencies of complement components or inhibitors and may be hereditary or acquired (see table Complement Deficiencies). Hereditary deficiencies are autosomal recessive except for deficiencies of C1 inhibitor, which is autosomal dominant, and properdin, which is X-linked. The deficiencies result in defective opsonization, phagocytosis, and lysis of pathogens and in defective clearance of antigen-antibody complexes.

The most serious consequences are

Recurrent infection, which is due to defective opsonization
Autoimmune disorders (eg, systemic lupus erythematosus, glomerulonephritis), which is due to defective clearance of antigen-antibody complexes

A deficiency in a complement regulatory protein causes hereditary angioedema.

Complement deficiencies can affect the classical and/or alternate pathways of the complement system. The alternate pathway shares C3 and C5 through C9 with the classical pathway but has additional components: factor D, factor B, properdin (P), and regulatory factors H and I.

For diagnostic evaluation of complement deficiencies, see tables Initial and Additional Laboratory Tests for Immunodeficiency and Specific and Advanced Laboratory Tests for Immunodeficiency.

Complement Deficiencies

Disorder	Inheritance	Clinical Findings
C1	Autosomal recessive	SLE
C2	Autosomal recessive	SLE, recurrent pyogenic infections with encapsulated bacteria (especially pneumococcal) that start in early childhood, other autoimmune disorders (eg, glomerulonephritis, polymyositis, vasculitis, IgA-associated vasculitis, Hodgkin lymphoma)
C3	Autosomal recessive	Recurrent pyogenic infections with encapsulated bacteria that start at birth, glomerulonephritis, other antigen-antibody complex disorders, sepsis
C4	Autosomal recessive	SLE, other autoimmune disorders (eg, IgA nephropathy, progressive systemic sclerosis, IgA-associated vasculitis, type 1 diabetes mellitus, autoimmune hepatitis)
C5, C6, C7, C8, C9 (membrane attack complex)	Autosomal recessive	Recurrent Neisseria meningitidis and disseminated N. gonorrhoeae infections
Complement deficiencies in the MBL pathway
MBL	Autosomal recessive	Recurrent pyogenic infections with encapsulated bacteria that start at birth; unexplained sepsis; increased severity of infection in secondary immunodeficiencies due to corticosteroid use, cystic fibrosis, or chronic lung disorders
MASP-2	Unknown	Autoimmune disorders (eg, inflammatory bowel disease, erythema multiforme), recurrent pyogenic infections with encapsulated bacteria (eg, Streptococcus pneumoniae)
Complement deficiencies in the alternative pathway
Factor B	Autosomal recessive	Pyogenic infections
Factor D	Autosomal	Pyogenic infections
Properdin	X-linked	Increased risk of fulminant neisserial infection
Complement regulatory protein deficiencies
C1 inhibitor	Autosomal dominant	Angioedema
Factor I	Autosomal codominant	Same as C3 deficiency
Factor H	Autosomal codominant	Same as C3 deficiency Hemolytic-uremic syndrome
Decay accelerating factor	Autosomal recessive	Paroxysmal nocturnal hemoglobinuria
Complement receptor (CR) deficiencies
CR1	Acquired	Secondary finding in immune (antigen-antibody) complex–mediated disease
CR3	Autosomal recessive	Leukocyte adhesion deficiency (recurrent Staphylococcus aureus and Pseudomonas aeruginosa infections)
C = complement; MASP = mannose-binding lectin-associated serine protease; MBL = mannose-binding lectin; SLE = systemic lupus erythematosus.

1. Picard C, Gaspar HB, Al-Herz W, et al: International Union of Immunological Societies: 2017 Primary Immunodeficiency Diseases Committee Report on Inborn Errors of Immunity. J Clin Immunol 38:96–128, 2018. doi: 10.1007/s10875-017-0464-9
2. Chinen J and Cowan MJ: Advances and highlights in primary immunodeficiencies in 2017. J Allergy Clin Immunol 142:1041–1051, 2018. doi: 10.1016/j.jaci.2018.08.016
3. Bonilla FA, Khan DA, Ballas ZK, et al: Practice parameter for the diagnosis and management of primary immunodeficiency. J Allergy Clin Immunol 136:1186–205, 2015. doi: 10.1016/j.jaci.2015.04.049. Epub 2015 Sep 12

Causes (see table Causes of Secondary Immunodeficiency) include

Systemic disorders (eg, diabetes, undernutrition, HIV infection)
Immunosuppressive treatments (eg, cytotoxic chemotherapy, bone marrow ablation before transplantation, radiation therapy)
Prolonged serious illness

Secondary immunodeficiency also occurs among critically ill, older, or hospitalized patients. Prolonged serious illness may impair immune responses; impairment is often reversible if the underlying illness resolves.

Causes of Secondary Immunodeficiency

Category	Examples
Endocrine	Diabetes mellitus
Gastrointestinal	Hepatic insufficiency, hepatitis, intestinal lymphangiectasia, protein-losing enteropathy
Hematologic	Aplastic anemia, cancers (eg, chronic lymphocytic leukemia, multiple myeloma, Hodgkin lymphoma), graft-vs-host disease, sickle cell disease, splenectomy
Iatrogenic	Certain drugs, such as chemotherapeutic drugs, immunosuppressants, corticosteroids; radiation therapy; splenectomy
Infectious	Viral infections (eg, cytomegalovirus, Epstein-Barr virus, HIV, measles virus, varicella-zoster virus), bacterial infections, rare bacterial infections with superantigens (antigens that can activate large numbers of T cells, resulting in massive cytokine production, most notably from Staphylococcus aureus), mycobacterial infections
Nutritional	Alcohol use disorder, undernutrition
Physiologic	Physiologic immunodeficiency in infants due to immaturity of the immune system, pregnancy
Renal	Nephrotic syndrome, renal insufficiency, uremia
Rheumatologic	Systemic lupus erythematosus
Other	Burns, cancers, chromosomal abnormalities (eg, Down syndrome), congenital asplenia, critical and chronic illness, histiocytosis, sarcoidosis

Some Drugs That Cause Immunosuppression

Class	Examples
Antiseizure drugs	Lamotrigine, phenytoin, valproate
Disease-modifying anti-rheumatic drugs (DMARDs)	Interleukin (IL)-1 inhibitors (eg, anakinra) IL-6 inhibitors (eg, tocilizumab) IL-17 inhibitors (eg, brodalumab) Tumor necrosis factor (TNF) inhibitors (eg, adalimumab, etanercept, infliximab) T-cell activation inhibitors (eg, abatacept, basiliximab) CD20 inhibitors (eg, rituximab) CD3 inhibitors (eg, muromonab-CD3) Janus kinase (JAK) inhibitors (eg, ruxolitinib)
Calcineurin inhibitors	Cyclosporine, tacrolimus
Corticosteroids	Methylprednisolone, prednisone
Cytotoxic chemotherapy drugs	Multiple (see Systemic Antineoplastic Therapy)
Purine metabolism inhibitors	Azathioprine, mycophenolate mofetil
Rapamycins	Everolimus, sirolimus
Immunosuppressive immunoglobulins	Antilymphocyte globulin, antithymocyte globulin

Immunodeficiency can result from loss of serum proteins (particularly IgG and albumin) through the following:

The kidneys in nephrotic syndrome
The skin in severe burns or dermatitis
The gastrointestinal (GI) tract in enteropathy

Enteropathy may also lead to lymphocyte loss, resulting in lymphopenia.

Treatment focuses on the underlying disorder; for example, a diet high in medium-chain triglycerides may decrease loss of immunoglobulins (Igs) and lymphocytes from the gastrointestinal tract and be remarkably beneficial.

If a specific secondary immunodeficiency disorder is suspected clinically, testing should focus on that disorder (eg, diabetes, HIV infection, cystic fibrosis, primary ciliary dyskinesia).

Some decrease in immunity occurs with aging. For example, in older adults, the thymus tends to produce fewer naive T cells; thus, fewer T cells are available to respond to new antigens. The total number of T cells does not decrease (because of oligoclonality), but these cells can recognize only a limited number of antigens.

Signal transduction (transmission of antigen-binding signal across the cell membrane into the cell) is impaired, making T cells less likely to respond to antigens. Also, helper T cells may be less likely to signal B cells to produce antibodies.

The number of neutrophils does not decrease, but these cells become less effective in phagocytosis and microbicidal action.

Undernutrition, common among older adults, impairs immune responses. Calcium, zinc, and vitamin E are particularly important to immunity. Risk of calcium deficiency is increased in older adults, partly because with aging, the intestine becomes less able to absorb calcium. Also, the elderly may not ingest enough calcium in their diet. Zinc deficiency is very common among adults living in institutional settings and homebound patients.

Certain disorders (eg, diabetes, chronic kidney disease, undernutrition), which are more common among older adults, and certain therapies (eg, immunosuppressants, immunomodulatory drugs and treatments), which the elderly are more likely to use, can also impair immunity.

Secondary (acquired) immunodeficiencies are much more common than primary (genetic) immunodeficiencies.
Primary immunodeficiencies can affect humoral immunity (most commonly), cellular immunity, both humoral and cellular immunity, phagocytic cells, or the complement system.
Patients who have primary immunodeficiencies may have nonimmune manifestations that can be recognized more easily than the immunodeficiencies.
Immunity tends to decrease with aging partly because of age-related changes; also, conditions that impair immunity (eg, certain disorders, use of certain drugs) are more common among older adults.

Drug Name	Select Trade
Methylprednisolone	MEDROL
mycophenolate	CELLCEPT
Azathioprine	IMURAN
Cyclosporine	NEORAL, SANDIMMUNE
ruxolitinib	JAKAFI
tocilizumab	ACTEMRA
Lamotrigine	LAMICTAL
basiliximab	SIMULECT
etanercept	ENBREL
infliximab	REMICADE
adalimumab	HUMIRA
tacrolimus	PROGRAF
prednisone	RAYOS
Everolimus	AFINITOR
brodalumab	Brodalumab
sirolimus	RAPAMUNE
phenytoin	DILANTIN
abatacept	ORENCIA
rituximab	RITUXAN
anakinra	KINERET

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