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Passive immunity

Passive immunity is a form of adaptive immunity in which pre-formed antibodies are transferred to an individual from another source, providing immediate but temporary protection against specific pathogens or toxins without activating the recipient's own immune system to produce antibodies.^[1] This contrasts with active immunity, where the body generates its own long-lasting immune response through exposure to antigens.^[2] Passive immunity typically lasts only a few weeks to several months, as the transferred antibodies are eventually degraded without replenishment.^[1] Passive immunity occurs naturally when maternal antibodies, primarily immunoglobulin G (IgG), cross the placenta to protect the fetus during pregnancy, or when secretory immunoglobulin A (IgA) is provided through colostrum and breast milk to safeguard the infant's gastrointestinal tract.^[2] These maternal antibodies can offer protection for 6 to 12 months after birth, depending on the pathogen and antibody levels.^[3] Artificially, passive immunity is induced by administering exogenous antibodies, such as through intravenous immunoglobulin (IVIG) derived from pooled human plasma or monoclonal antibodies produced in laboratories.^[4] The mechanisms of passive immunity primarily involve antibody-mediated effects, including neutralization of pathogens or toxins to prevent their attachment to host cells, opsonization to enhance phagocytosis by immune cells, and activation of the complement system for pathogen destruction.^[4] Discovered in the late 19th century by Emil von Behring and Shibasaburo Kitasato through experiments with diphtheria antitoxins, passive immunization laid the foundation for modern antibody therapies.^[4] Clinically, passive immunity is used for immediate prophylaxis or treatment in high-risk scenarios, such as administering tetanus antitoxin after wound exposure, rabies immunoglobulin post-bite, or monoclonal antibodies such as palivizumab or nirsevimab to prevent respiratory syncytial virus (RSV) in infants.^[3] It is particularly valuable for immunocompromised individuals or during outbreaks, including the COVID-19 pandemic, though it does not confer immunological memory and must often be combined with active vaccination for sustained protection.^[1] Advances in monoclonal antibody production have expanded its applications to combat emerging infections and antibiotic-resistant pathogens.^[4]

Overview and mechanisms

Definition and basic principles

Passive immunity is the process by which an individual acquires immediate but temporary protection against a pathogen through the direct transfer of pre-formed antibodies from an immunized donor, without stimulating the recipient's own immune system to produce antibodies.^[5] This form of immunity primarily involves humoral components, such as antibodies, providing short-term defense until the transferred antibodies are naturally degraded or cleared.^[4] Key characteristics of passive immunity include its transient nature, typically lasting from several weeks to three or four months, depending on the type and dose of transferred antibodies like IgG or IgA, which have varying half-lives in the body.^[4] Unlike other immune responses, it does not generate immunological memory, meaning the recipient remains susceptible to the pathogen once the borrowed protection diminishes, as no endogenous memory cells are formed.^[2] The foundational observation of passive immunity occurred in 1890, when Emil von Behring and Shibasaburo Kitasato demonstrated that serum containing antitoxins from animals immunized against diphtheria and tetanus could confer protection to uninfected animals, marking the first experimental evidence of antibody transfer for therapeutic purposes.^[6] In comparison, active immunity arises from the recipient's direct exposure to an antigen, which triggers the endogenous production of antibodies and the development of long-lasting memory cells, providing prolonged protection.^[1] Passive immunity can be acquired through natural or artificial means, though its mechanisms and applications vary accordingly.^[7]

Biological mechanisms of antibody transfer

Passive immunity relies primarily on the transfer of immunoglobulins, particularly IgG and IgA, from a donor to a recipient, enabling immediate protection without stimulating the recipient's adaptive immune response. IgG is the dominant antibody class involved in systemic passive immunity due to its ability to cross biological barriers and its extended half-life of approximately 21 days, which allows sustained circulation in the recipient.^[8] In contrast, IgA, especially in its secretory form (sIgA), plays a key role in mucosal passive immunity, providing localized protection at epithelial surfaces such as the gastrointestinal tract.^[9] The transplacental transfer of IgG occurs through an active, receptor-mediated process in the placenta. Maternal IgG binds to the neonatal Fc receptor (FcRn) on the apical surface of syncytiotrophoblast cells via its Fc region, followed by endocytosis into endosomes where pH-dependent release facilitates transcytosis to the fetal circulation.^[10] This mechanism ensures selective transport of IgG subclasses, with IgG1 and IgG4 exhibiting higher efficiency due to stronger FcRn affinity.^[11] For IgA transfer, maternal plasma cells in the mammary glands produce dimeric IgA, which is transported across epithelial cells into colostrum and breast milk via the polymeric immunoglobulin receptor (pIgR), forming sIgA that resists proteolytic degradation in the infant's gut.^[12] Once transferred, these antibodies exert effector functions to combat pathogens in the recipient. IgG facilitates neutralization by binding to viral or bacterial antigens, preventing their attachment to host cells, and promotes opsonization by coating pathogens to enhance phagocytosis via Fcγ receptors on immune cells.^[13] Additionally, IgG activates the classical complement pathway, leading to pathogen lysis and further amplification of inflammation.^[14] Secretory IgA, meanwhile, neutralizes pathogens at mucosal sites through immune exclusion, agglutinating microbes and inhibiting their adhesion to epithelial cells without triggering systemic inflammation.^[15] In newborns receiving transplacental IgG, antibody levels typically peak at birth, reflecting maternal concentrations, and follow an exponential decay curve, declining to negligible levels over 6-12 months as the infant's own production matures.^[16] This waning is governed by the IgG half-life and catabolic rates, with faster clearance observed in the early postnatal period due to immature FcRn expression in the infant.^[17] The efficacy of transferred antibodies depends on several physiological factors. Higher maternal antibody doses correlate with greater peak levels and prolonged protection in the recipient, while antibody affinity to FcRn influences transfer efficiency, with suboptimal glycosylation or subclass variations reducing uptake.^[18] Recipient age at transfer impacts duration, as preterm infants exhibit lower absolute IgG levels due to reduced gestational exposure time.^[16] Underlying health conditions, such as placental pathologies or infant malnutrition, can further impair transfer or accelerate antibody clearance, diminishing overall protective outcomes.^[10]

Natural passive immunity

Maternal passive immunity

Maternal passive immunity primarily occurs through the transplacental transfer of immunoglobulin G (IgG) antibodies from the mother's bloodstream to the fetal circulation, a process that begins as early as 13 weeks of gestation and increases linearly thereafter.^[10] This transfer is mediated by the neonatal Fc receptor (FcRn) on syncytiotrophoblast cells in the placenta, which actively transports maternal IgG across the barrier.^[19] By 28–32 weeks of gestation, fetal IgG levels reach approximately 50% of maternal concentrations, with the majority of transfer occurring in the third trimester; at term birth, fetal levels often equal or exceed maternal IgG by 100–120%, providing robust humoral protection against systemic infections.^[10] ^[20] This passive immunity shields the neonate from pathogens such as tetanus and measles during the initial months of life when their own antibody production is immature.^[16] In addition to transplacental transfer, breastfeeding delivers secretory immunoglobulin A (sIgA) via colostrum and mature milk, which coats the infant's gastrointestinal mucosa to prevent adhesion and invasion by enteric pathogens.^[21] Colostrum, produced in the first few days postpartum, is particularly rich in sIgA, offering localized protection against viruses like rotavirus and bacteria such as Escherichia coli and Shigella.^[22] Unlike IgG, sIgA in breast milk is resistant to proteolytic degradation in the acidic infant gut, ensuring its stability and efficacy at mucosal surfaces for immune exclusion.^[23] The duration of maternal IgG-mediated protection typically wanes after 6 months as these antibodies are gradually catabolized, with half-life estimates around 21–28 days, leaving infants vulnerable until active immunization takes effect.^[17] This transient immunity is especially critical in regions with low vaccination coverage, where it serves as the primary defense against vaccine-preventable diseases in early infancy.^[24] Transfer efficiency varies between term and preterm infants; term neonates receive higher absolute IgG levels due to longer exposure during gestation, while preterm infants often have reduced concentrations, increasing their susceptibility to infections.^[25] Maternal vaccination, such as a pertussis booster in the third trimester, enhances cord blood IgG levels against specific pathogens, thereby augmenting neonatal protection.^[26]

Other natural transfers

In certain avian species, such as pigeons and doves, passive immunity is transferred naturally to offspring through crop milk, a nutrient-rich secretion produced by the epithelial lining of the parents' crop. This milk contains immunoglobulins, including IgA and IgG, which provide newborns with immediate protection against pathogens during their vulnerable early stages.^[27] Studies have demonstrated that these antibodies in crop milk are absorbed by squabs within the first day of life, contributing to immune defense against infections like West Nile virus.^[28] This mechanism is particularly significant in columbiform birds, where both parents produce crop milk, enhancing the transfer of maternal and paternal antibodies to support chick survival.^[29] In veterinary contexts, passive immunity via colostrum ingestion plays a vital role in livestock, especially in species like cattle where newborns lack transplacental antibody transfer. Neonatal calves must consume colostrum within the first few hours after birth to absorb immunoglobulins, primarily IgG, which confer protection against common enteric pathogens such as Escherichia coli.^[30] Failure to achieve adequate passive transfer increases the risk of scours and mortality, with studies showing that colostrum-derived antibodies control E. coli colonization in the gut and bolster innate immune responses.^[31] This process is time-sensitive, as the calf's intestinal epithelium closes to large-molecule absorption after approximately 24 hours, limiting efficiency if delayed.^[32] These natural transfers outside typical human maternal contexts are often species-specific, relying on direct ingestion or absorption mechanisms that provide short-term immunity but require timely execution for effectiveness. In non-human animals, such as birds and ruminants, they highlight adaptive strategies for neonatal protection, though they are less reliable in humans due to the dominance of placental and lactational routes.^[33]

Artificial passive immunity

Historical development

The concept of artificial passive immunity emerged in the late 19th century through pioneering experiments demonstrating that serum from immunized animals could transfer protective antibodies to treat infectious diseases. In 1890, Emil von Behring and Shibasaburo Kitasato reported the discovery of diphtheria antitoxin, showing that serum from animals immunized against diphtheria toxin neutralized the pathogen's effects in animal models, marking the first successful application of serum therapy.^[34]^[35] Their work built on earlier observations of natural antibody transfer but focused on harnessing animal-derived antitoxins for therapeutic use. For this breakthrough in serum therapy, particularly against diphtheria, Behring was awarded the first Nobel Prize in Physiology or Medicine in 1901.^[36] Early clinical applications followed rapidly, with the first human trials of diphtheria antitoxin conducted in 1894 at institutions in Berlin, where 220 children received injections, achieving a survival rate of 76% compared to historical mortality exceeding 50%.^[37] Serum therapy was extended to tetanus shortly after, with antitoxin introduced in clinical practice by 1891, and to scarlet fever by 1900, when horse-derived serum developed in Vienna reduced case fatality rates from around 20-30% to lower levels during outbreaks.^[38]^[39] These treatments proved vital during epidemics, saving thousands of lives; for instance, diphtheria antitoxin dramatically lowered mortality in the United States from over 40% to under 10% by the early 1900s, transforming management of these bacterial infections.^[40]^[41] Despite these successes, challenges arose from adverse reactions to animal sera, particularly horse-derived products. In 1905, Clemens von Pirquet and Béla Schick identified serum sickness, an immune complex-mediated hypersensitivity reaction characterized by fever, rash, and arthralgia occurring 7-14 days after injection, affecting up to 50% of recipients in early trials. This complication prompted efforts to mitigate risks, leading to a shift toward human-derived sera in the 1930s through methods like ammonium sulfate precipitation to isolate immunoglobulins from pooled human plasma, reducing foreign protein exposure.^[42] Key milestones in the mid-20th century included the 1940s development of gamma globulin, a concentrated human immunoglobulin fraction produced via ethanol fractionation of plasma, first used successfully by Charles Janeway for measles prophylaxis, preventing severe disease in exposed children with doses of 0.1-0.25 mL/kg.^[43] Post-World War II standardization efforts, including U.S. regulatory guidelines and large-scale production from donor plasma pools, ensured safer, more consistent preparations, paving the way for broader prophylactic use against viral infections like measles and hepatitis.^[44]^[43]

Modern applications and therapies

Intravenous immunoglobulin (IVIG) and intramuscular immunoglobulin (IMIG) are key components of modern passive immunity therapies, primarily used to treat primary immunodeficiencies and provide prophylaxis against certain infections. For patients with primary immunodeficiency diseases, IVIG is administered at replacement doses of 400–600 mg/kg body weight every 3–4 weeks to maintain adequate antibody levels and prevent recurrent infections.^[45] In cases of hepatitis A exposure, IMIG is recommended for postexposure prophylaxis at a dose of 0.1 mL/kg intramuscularly, ideally within 2 weeks of exposure, to confer immediate protection in individuals for whom vaccination is contraindicated or unavailable.^[46] Monoclonal antibodies represent a significant advancement in targeted passive immunity, offering precise and potent neutralization of pathogens. Nirsevimab (trade name Beyfortus), approved by the FDA in July 2023, is a long-acting monoclonal antibody for preventing respiratory syncytial virus (RSV) lower respiratory tract disease in infants. Administered as a single intramuscular dose—50 mg for infants weighing less than 5 kg or 100 mg for those 5 kg or more—it provides protection for at least five months, covering the typical RSV season. As of 2025, CDC recommends nirsevimab for all infants younger than 8 months entering their first RSV season, with expanding access programs in 2024–2025.^[47]^[48] Other established applications include postexposure prophylaxis for rabies and treatment of botulism. For rabies, human rabies immune globulin (HRIG) is given at 20 IU/kg body weight on day 0 alongside the rabies vaccine to provide immediate neutralizing antibodies against the virus in unvaccinated individuals.^[49] In botulism cases, equine-derived heptavalent botulism antitoxin is administered intravenously to neutralize circulating toxin, reducing mortality when given early in the course of illness.^[50] During the early COVID-19 pandemic, monoclonal antibodies like sotrovimab were authorized for emergency use in mild-to-moderate cases in high-risk patients, but their efficacy has been limited by SARS-CoV-2 variants, leading to revocation of authorization in regions with predominant resistant strains.^[51] Emerging therapies focus on broad-spectrum monoclonal antibodies to address evolving threats from viruses like influenza and Ebola. For influenza, clinical trials are evaluating broadly neutralizing antibodies that target conserved viral epitopes, aiming to provide universal protection across strains with single-dose administration.^[52] Similarly, antibody cocktails such as ZMapp, composed of three monoclonal antibodies against Ebola glycoprotein, have demonstrated efficacy in preclinical and early clinical studies for postexposure prophylaxis and treatment, highlighting the potential for rapid deployment in outbreaks. As of 2025, new long-acting RSV monoclonal antibodies like clesrovimab are in advanced clinical trials, potentially offering alternatives to nirsevimab for infant prophylaxis.^[53]^[54]

Cell-mediated passive immunity

Mechanisms of T-cell transfer

Passive cell-mediated immunity is achieved through the adoptive transfer of primed T lymphocytes or cytokine-activated immune cells from a donor to a recipient, conferring immediate effector functions without requiring the recipient's own immune priming. This process, first conceptualized in the mid-20th century, enables the recipient to mount a targeted response against intracellular threats such as viruses or tumors by leveraging the transferred cells' pre-existing specificity and activation state.^[55]^[56] Donor-derived T cells for transfer are typically sourced from peripheral blood, tumor-infiltrating lymphocytes, draining lymph nodes, or as passenger cells in allogeneic stem cell grafts. These cells are often isolated and expanded in vitro using cytokines like interleukin-2 (IL-2) to generate sufficient numbers for infusion, ensuring they retain antigen specificity and effector potential prior to administration. Upon transfer, the T cells home to target tissues via chemokine gradients, such as those mediated by CXCR3 and CCR5 receptors, allowing migration to sites of infection or malignancy.^[56]^[57]^[58] Once at the site, transferred T cells recognize antigens presented on major histocompatibility complex (MHC) molecules via their T cell receptors (TCRs), triggering activation and downstream effector responses. This includes the release of cytokines such as interferon-gamma (IFN-γ), which activates macrophages and enhances antigen presentation, as well as cytotoxic molecules like perforin and granzymes that directly lyse infected or malignant cells. Unlike humoral passive immunity, which relies on antibody neutralization of extracellular pathogens, T-cell transfer primarily targets intracellular antigens through cell-mediated cytotoxicity, providing protection against threats inaccessible to antibodies. The persistence of these transferred T cells is generally short-term, lasting days to weeks, due to their effector phenotype and lack of recipient-generated memory, though strategies like lymphodepletion can extend this duration.^[56]^[58]^[59]

Clinical examples and limitations

One prominent clinical example of cell-mediated passive immunity is the graft-versus-tumor (GVT) effect observed in allogeneic bone marrow transplants for leukemia treatment, where donor T cells transferred via hematopoietic stem cell transplantation recognize and eliminate residual leukemic cells.^[60] This GVT effect contributes to improved relapse-free survival in acute myeloid leukemia patients post-transplant, particularly when T-cell depletion is minimized to preserve donor immunity.^[61] Chimeric antigen receptor (CAR) T-cell therapy represents another key application, involving the infusion of patient-derived or donor-engineered T cells that passively confer antitumor immunity against hematologic malignancies. For instance, tisagenlecleucel, approved by the FDA in 2017 for relapsed or refractory B-cell acute lymphoblastic leukemia, delivers pre-engineered CD19-targeted T cells that persist and exert cytotoxic effects without requiring active host immunization.^[62] Clinical trials have demonstrated complete remission rates exceeding 80% in pediatric and young adult patients, highlighting its efficacy as a passive transfer mechanism.^[58] In infectious diseases, experimental T-cell transfers have been employed to combat cytomegalovirus (CMV) reactivation in transplant recipients, where donor-derived CMV-specific T cells are adoptively infused to provide immediate antiviral protection. Studies in hematopoietic stem cell transplant patients have shown that such transfers can resolve refractory CMV viremia with response rates up to 70%, though routine use remains limited due to logistical complexities in cell isolation and expansion.^[63] A 2025 review confirms ongoing evaluation primarily in high-risk adult cohorts, with prophylactic applications still investigational.^[64] Despite these advances, cell-mediated passive immunity faces significant limitations, including the risk of graft-versus-host disease (GVHD) in allogeneic transfers, where donor T cells attack host tissues, occurring in 30-50% of cases and necessitating immunosuppressive management.31829-3/fulltext) Transferred T cells often exhibit short persistence, typically lasting weeks to months, which may require repeated dosing to maintain efficacy against persistent threats like tumors or chronic infections. High manufacturing costs, exceeding $400,000 per CAR-T infusion, restrict accessibility, compounded by the need for specialized facilities.^[58] Ethical concerns also arise in donor sourcing, such as mobilization protocols that could pose health risks to healthy volunteers.^[65] As of 2025, cell-mediated passive immunity primarily serves as an adjunct in multimodal immunotherapy regimens, such as combining CAR-T with checkpoint inhibitors for enhanced antitumor responses, rather than a standalone prophylactic strategy comparable to antibody-based approaches.^[66]

Advantages and disadvantages

Advantages

Passive immunity offers immediate protection upon antibody transfer, typically within hours, making it particularly valuable for individuals recently exposed to pathogens or those unable to mount a rapid immune response.^[1] This rapid onset contrasts with active immunity, which requires days to weeks for antibody production, allowing passive approaches to serve as an urgent intervention in high-risk scenarios.^[4] For immunocompromised patients, such as those with HIV, passive immunization provides essential short-term defense when endogenous immunity is impaired.^[67] Newborns, who receive maternal antibodies transplacentally, exemplify this benefit, gaining protection against infections before their own immune systems mature.^[68] In outbreak settings, passive immunity acts as a bridge to active immunization, delivering prompt coverage while vaccines take effect. For instance, intramuscular immunoglobulin (IG) administered within six days of measles exposure prevents or modifies disease in unvaccinated individuals, buying time for vaccination to confer long-term protection.^[69] This strategy is especially useful during epidemics, where immediate intervention can curb transmission among susceptible populations.^[70] Monoclonal antibodies (mAbs) used in passive therapy provide highly targeted protection, binding specific pathogen epitopes to neutralize threats with minimal impact on the host's normal flora. This specificity results in lower toxicity and fewer side effects compared to broad-spectrum antimicrobials, which can disrupt beneficial microbes and lead to resistance or secondary infections.^[50] For example, RSV mAbs like nirsevimab and, as of June 2025, clesrovimab offer precise, immediate shielding for high-risk infants without the broader disruptions of antibiotics.^[71]^[72] Passive immunity is particularly safe for vulnerable groups, such as infants and the elderly, as it involves pre-formed antibodies rather than live or attenuated pathogens, eliminating the risk of vaccine-induced disease.^[73] In infants, whose immature immune systems may not tolerate live vaccines, this approach avoids potential adverse reactions while providing critical early protection.^[74] Similarly, for elderly individuals with waning immunity, passive transfer circumvents the challenges of vaccine responsiveness without introducing infection risks.^[75]

Disadvantages

Passive immunity provides only temporary protection, as transferred antibodies are eventually catabolized without inducing the recipient's own immune response or memory cells. The half-life of immunoglobulin G (IgG), the primary antibody class used in passive immunization, averages 21 days in humans, leading to a gradual decline in antibody levels and protection that typically lasts only a few weeks to months.^[76]^[77] For extended half-life mAbs like nirsevimab, real-world data as of November 2025 suggest protection may extend up to 1 year, though repeat dosing may still be needed in high-risk areas.^[78] This short duration necessitates repeated administrations or boosters to maintain efficacy, unlike active immunity which establishes long-term defense.^[79] A significant drawback involves potential adverse effects, particularly from the use of heterologous (non-human) sera in early passive immunization therapies. These can trigger allergic reactions or immune complex diseases such as serum sickness, a type III hypersensitivity response characterized by fever, rash, joint pain, and lymphadenopathy occurring 7-14 days post-administration.^[80]^[81] Although modern monoclonal antibodies (mAbs) derived from human or engineered sources have reduced these risks, hypersensitivity remains a concern in some recipients.^[82] The high cost of producing monoclonal antibodies limits accessibility, especially in resource-constrained settings. For instance, a single dose of nirsevimab, a long-acting mAb for respiratory syncytial virus prevention in infants, costs approximately $500 in the United States, contributing to economic barriers for widespread use.^[83] While supply chain disruptions exacerbated shortages during the COVID-19 pandemic, for RSV mAbs, initial shortages in 2023-2024 have been addressed, with no shortages expected for 2025-2026 due to increased production and the approval of additional therapies.^[84]^[85] Passive immunity is often strain-specific, offering limited protection against viral variants due to the narrow targeting of transferred antibodies. This was evident in the COVID-19 pandemic, where several authorized mAbs, such as sotrovimab and Evusheld, lost efficacy against the Omicron variant and its sublineages, prompting the FDA to revoke or limit their emergency use authorizations.^[51]^[86]^[87]

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