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Reactive lymphocyte
Reactive lymphocyte
Reactive lymphocyte
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Reactive lymphocyte surrounded by red blood cells

In immunology, reactive lymphocytes, variant lymphocytes, atypical lymphocytes, Downey cells or Türk cells are cytotoxic (CD8+) lymphocytes that become large as a result of antigen stimulation. Typically, they can be more than 30 μm in diameter with varying size and shape.

Discovery

Reactive lymphocytes were originally described by W. Türk in 1907 in the peripheral blood of patients with infectious mononucleosis. Later in 1923 the features of the reactive lymphocytes were characterized in greater detail by Hal Downey and C.A. McKinlay, who also discovered the association with EBV and CMV.[1][2]

Morphology

[edit]

Downey and McKinlay first described the atypical lymphocytes seen in cases of infectious mononucleosis. They further categorized the atypical lymphocytes of different etiologies under three subtypes:[3]

  1. Type I as highly differentiated "leukocytoid lymphocyte", round-to-lobulated nucleus, mature clumped chromatin with or without nucleoli and with varying degree of basophilia in the cytoplasm.
  2. Type II as larger cells with round-to-lobulated nucleus, chromatin resembling that of plasma cells, moderate amount of cytoplasm with mild basophilia.
  3. Type III cells are large cells with a round to slightly indented nucleus, chromatin mostly immature with diffuse sieve-like arrangements and nucleoli.

Downey type II cell is the most common type of reactive lymphocyte. In general, those cells may vary in morphologic detail as well as surface marker characteristics since this is the result of a polyclonal immune response to antigenic stimulation. All three types of Downey cells were observed along with some other variants such as larger cells with deeply convoluted nucleus, cells with crystalline rods and granules in the cytoplasm, flame cells, Mott cells, and some intermediate forms.[4] Flame cells are plasma cells characterized by a pink fringe of cytoplasm, often observed in the bone marrow of cats, especially in conditions such as multiple myeloma and chronic infections.[5]

The common features of reactive lymphocytes:[6]

  • larger than normal size, sometimes with a diameter of more than 30 microns;
  • nucleus can be round, elliptic, indented, cleft, or folded;
  • the cytoplasm is often abundant and can be basophilic – most often, the cytoplasm is gray, pale blue, or deep blue in color;
  • vacuoles and/or azurophilic granules are also sometimes present;
  • histochemistry shows increased concentrations of acid phosphatase, phosphorylase, and non-specific esterase;
  • prominent clusters and rosettes of free ribosome;
  • presence of small vacuoles near the edge of the cytoplasm as well as invaginations in the cell surface.

Molecular markers

[edit]

Atypical lymphocyte population often express features of activated CD8+ T cells, such as CD29, CD38, HLA-DR, CD45RO and CD95. Expression of CD25 was on the other hand decreased.[7]

Expressed molecular markers may vary depending on many factors. For example, CD57 expression seems to be significantly decreased only in patients with EBV infections.[7]

Function

[edit]

The atypical lymphocytes have been best studied from blood of patients with infectious mononucleosis. Early studies suspect that atypical lymphocytes could have both T or B cells features; now it is more suggested that reactive lymphocytes are activated T-lymphocytes produced in response to infected B-lymphocytes.[8][6]

Reactive lymphocytes have been found to accumulate in areas of inflammation like the liver and pharynx of individuals with infectious mononucleosis and skin window preparations. In infectious mononucleosis, the atypical lymphocytes are one component of a normal immune system that helps to control potentially fatal Epstein-Barr virus-induced B-cell lymphoma in human.

Causes

[edit]

Reactive lymphocytes are usually associated with viral illnesses, but they can also be present as a result of drug reactions (such as phenytoin), immunizations, radiation, and hormonal causes (such as stress and Addison's disease), as well as some autoimmune disorders (such as rheumatoid arthritis).[8]

Some pathogen-related causes include:[7]

Association with COVID-19

[edit]

The presence of Downey cells were observed in many COVID-19 cases, together with the atypical plasmacytoid lymphocytes (which could be one of the less usual atypical lymphocyte types).[10][11]

Some observations even suggest that the presence of particular reactive lymphocytes in some of the infected patients could be an indicator of a better prognosis of the disease.[12]

See also

[edit]

References

[edit]
[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Reactive lymphocyte

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from Grokipedia
A reactive lymphocyte, also known as an lymphocyte, is a morphologically altered in the peripheral blood that arises as part of the immune system's response to antigenic stimulation, such as infections or other stressors. These cells are typically non-neoplastic and polyclonal, reflecting activation of T or B s rather than , and they play a key role in mounting an adaptive immune defense. Reactive lymphocytes exhibit heterogeneous morphology, distinguishing them from normal small lymphocytes. They vary in size (often larger than typical lymphocytes), with features including irregular, scalloped, or cleaved nuclei, clumped , occasional prominent nucleoli, and abundant, deeply basophilic that may appear foamy or vacuolated. Some subtypes, such as immunoblast-like cells, show high nuclear-to-cytoplasmic ratios and condensed , while others resemble Downey type II cells with pale blue that may indent adjacent erythrocytes. These changes result from upregulated protein synthesis, including immunoglobulins and inflammatory mediators, during blast transformation. The presence of reactive lymphocytes is most commonly associated with viral infections, including Epstein-Barr virus (causing ), cytomegalovirus, HIV, and hepatitis viruses, as well as bacterial infections like pertussis or . Other causes include drug reactions (e.g., or DRESS syndrome), autoimmune disorders, stress responses such as epinephrine release from trauma or excitement, recent vaccinations, and chronic antigenic stimulation. In clinical practice, their identification on peripheral blood smears is crucial for differentiating benign reactive processes from like or , often requiring correlation with patient history, absolute lymphocyte counts, and sometimes or repeat testing. While usually transient and resolving with the underlying stimulus, persistent or marked reactive may warrant further investigation to rule out malignancy.

Introduction and History

Definition

Reactive lymphocytes, also known as atypical lymphocytes, are non-neoplastic lymphocytes that undergo morphological and functional transformation in response to antigenic stimulation, representing a benign activation of the adaptive immune system. These cells primarily consist of activated T lymphocytes, particularly CD8+ T cells in contexts like viral infections, but can also include activated B lymphocytes depending on the stimulus. Unlike malignant transformations, this process involves polyclonal expansion without genetic aberrations, serving as a normal physiological response to pathogens or other antigens. Key characteristics of reactive lymphocytes include increased cell size (often 15–30 micrometers), irregular or indented nuclei, abundant basophilic that may contain vacuoles, and expression of activation markers such as CD25 () and , which signify ongoing immune engagement without neoplastic intent. These features reflect blast-like transformation from small resting precursors, enabling enhanced effector functions like production and . In distinction to resting lymphocytes, which are small (7-10 micrometers) with round nuclei and scant cytoplasm, reactive lymphocytes exhibit dynamic structural changes indicative of rather than quiescence. Malignant lymphocytes, conversely, demonstrate monoclonal proliferation, aberrant immunophenotypes (e.g., loss of pan-T or B markers), and cytogenetic abnormalities, contrasting the polyclonal, reversible nature of reactive forms.

Historical Discovery

The recognition of reactive lymphocytes began with advancements in histological staining techniques developed by in the late , which enabled the differentiation and visualization of various blood cell types, including lymphocytes, under the . These methods, refined through the early , laid the groundwork for identifying morphological variations in peripheral blood smears during infections. By , Wilhelm Türk described atypical mononuclear cells in the blood of patients with , marking one of the earliest observations of what would later be recognized as reactive lymphocytes. In 1923, hematologists Hal Downey and C.A. McKinlay provided a seminal classification of these atypical lymphocytes observed in , categorizing them into three types based on morphological features seen in blood smears—Type I (small with scant ), Type II (plasmacytoid with abundant ), and Type III (large with indented nuclei)—and associating them with acute infectious processes. This work highlighted their transient nature in response to infection rather than . Key progress in the 1930s and 1940s came from serological studies linking these cells to viral infections, notably through John R. Paul and Walls W. Bunnell's 1932 identification of heterophile antibodies in patients, which suggested an immune-mediated viral etiology and correlated with the presence of atypical lymphocytes. The formal term "reactive lymphocyte" emerged in mid-20th century literature as pathologists distinguished these activated cells from leukemic forms, emphasizing their role in non-neoplastic immune responses. Post-World War II advances in further solidified this understanding, with studies in the 1950s and 1960s associating the cells with antigen-driven activation in viral contexts, paving the way for their characterization as part of adaptive immunity.

Morphological Characteristics

Light Microscopy Features

Reactive lymphocytes exhibit distinctive morphological features observable under light microscopy, particularly when stained with Wright-Giemsa, distinguishing them from resting lymphocytes. These activated cells are typically larger than normal small lymphocytes, measuring 10-25 μm in diameter, with a nuclear-to-cytoplasmic (N:C) ranging from 3:1 to 1:2. Their shapes vary heterogeneously, appearing round, ovoid, indented, cleft, or irregular, often molded by adjacent erythrocytes, which imparts a characteristic "skirting" or amoeboid contour to the cell margins. The in reactive lymphocytes is abundant and basophilic, staining deep blue with Wright-Giemsa, reflecting increased content from . It may appear foamy, vacuolated, or contain rare azurophilic granules, and in some variants, a perinuclear clear zone (hof) is evident, mimicking morphology. Nuclear features include eccentric or indented positioning, with irregular contours, coarse to moderately clumped , and occasional small nucleoli, particularly in immunoblastic forms. Plasmacytoid variants show eccentric nuclei with clock-face patterns, while immunoblast-like cells display more dispersed and prominent nucleoli. In peripheral blood smears during an , reactive lymphocytes typically constitute 5-20% of the total population, though percentages can exceed this in intense stimuli like viral infections.

Immunophenotypic and Molecular Markers

Reactive lymphocytes, primarily T cells in most cases, typically express CD3 as a pan-T cell marker, with subsets showing either or co-expression, distinguishing them from other leukocyte populations. Upon , these cells upregulate early and late markers such as for initial , CD25 ( alpha chain) for proliferation signaling, and for enhancement, which are detected via multicolor panels to confirm reactive status. In B-cell reactive variants, such as those seen in polyclonal B-cell , surface immunoglobulin expression is polytypic, showing a balanced kappa:lambda ratio without light chain restriction, contrasting with monoclonal B-cell proliferations. At the molecular level, reactive lymphocytes demonstrate upregulation of activation-associated genes, including those encoding the (CD25) and interferon-gamma, reflecting a broad rather than neoplastic transformation. Critically, they lack clonal rearrangements in (IGH) or (TCR) genes, as assessed by PCR-based clonality studies, yielding polyclonal or Gaussian banding patterns that rule out . Flow cytometry remains the gold standard for immunophenotyping peripheral blood or bone marrow samples, using antibody panels targeting CD3, , , , CD25, and to identify heterogeneous, non-clonal populations of activated lymphocytes. For tissue biopsies, immunohistochemistry highlights these markers in situ, revealing a diverse mix of activated T and B cells without aberrant loss or aberrant co-expression seen in malignancies.

Biological Function

Role in Immune Response

Reactive lymphocytes play a central role in the adaptive by undergoing antigen-specific proliferation upon recognition of foreign pathogens, enabling a targeted expansion of clones to mount an effective defense. This proliferation allows for the amplification of antigen-specific T and B cells, which differentiate into effector cells capable of production to orchestrate and recruit other immune components. For instance, activated CD4+ helper T cells secrete cytokines such as interleukin-2 (IL-2) and interferon-gamma (IFN-γ) to enhance the response against intracellular pathogens. Concurrently, CD8+ cytotoxic T cells mediate direct cell killing through perforin and granzyme release, eliminating infected host cells, while helper T cells provide support to B cells for production, neutralizing extracellular threats like viruses and . These reactive lymphocytes interact closely with innate immune cells to amplify the overall response, collaborating with macrophages to enhance and , as well as with natural killer (NK) cells to bridge innate and adaptive immunity in lymph nodes. During systemic infections, reactive lymphocytes undergo rapid expansion primarily in secondary lymphoid organs such as lymph nodes, primarily in T-cell zones for T lymphocytes and in germinal centers within B-cell follicles for B lymphocytes, to facilitate proliferation and differentiation, before disseminating into the blood to reach infection sites. This expansion contributes to temporary , where lymphocytes can constitute up to 50% of , providing a surge in effector cells for rapid clearance. The outcomes of reactive lymphocyte activation include resolution of infections through the formation of effector memory cells, which persist long-term to confer faster responses upon re-exposure to the same . The polyclonal nature of this expansion— involving diverse clones specific to multiple epitopes—ensures a broad, non-dominant response that maintains and minimizes the risk of by avoiding over-reliance on potentially self-reactive clones.

Activation Mechanisms

Reactive lymphocytes, encompassing both T and B cells, initiate activation through recognition by their respective receptors. In T cells, the (TCR) binds to peptide antigens presented by (MHC) molecules on antigen-presenting cells, forming the that triggers initial signaling. is essential to prevent anergy, achieved via the interaction of on T cells with B7-1 () and B7-2 () ligands on antigen-presenting cells, amplifying TCR signals and promoting survival and proliferation. For B cells, the (BCR), composed of membrane-bound immunoglobulin and associated signaling chains, directly recognizes soluble or membrane-bound antigens, leading to receptor clustering and internalization for processing. B cell often involves CD40 ligand from helper T cells interacting with CD40 on B cells, enhancing BCR-mediated responses and facilitating formation. Upon recognition, intracellular signaling cascades propagate the activation signal, culminating in cellular proliferation and differentiation. In both T and B cells, BCR and TCR engagement activates tyrosine kinases such as Src family members (e.g., Lck in T cells, Lyn in B cells), leading to of adaptor proteins and recruitment of phospholipase Cγ, which generates second messengers like IP3 and DAG. These initiate the pathway, where phosphorylates IκB, allowing translocation to the nucleus to transcribe genes for survival and proliferation, and the MAPK/ERK pathway, which promotes entry via AP-1 and Elk-1 transcription factors. Cytokines play a in sustaining these cascades; for instance, IL-2 in T cells activates JAK-STAT pathways to further amplify and MAPK activity, driving clonal expansion, while IFN-γ enhances MHC expression and sustains effector functions in both T and B cells. The transformation process converts naive lymphocytes into reactive effector states, marked by blast formation and functional differentiation. Naive T cells, upon activation, undergo blast transformation, enlarging and increasing content to enter the , progressing from G0 to within hours and proliferating into effector subsets like cytotoxic or helper T cells. Similarly, naive B cells transform into plasmablasts or memory B cells, with increased metabolic activity and secretion, driven by sustained signaling and support. This differentiation involves epigenetic changes and transcription factors such as T-bet for Th1 effectors or Blimp-1 for plasma cells, enabling specialized immune functions. To prevent excessive expansion, activation is tightly regulated by apoptosis pathways, particularly via Fas/ interactions. Activated T cells upregulate Fas (CD95) and (FasL), and upon re-encountering or receiving high-dose stimulation, FasL trimerizes Fas, recruiting and to form the death-inducing signaling complex (DISC), initiating extrinsic . This activation-induced cell death (AICD) limits effector populations post-resolution, maintaining immune homeostasis, with similar mechanisms operating in B cells to control reactions. Markers such as increased and expression briefly indicate early activation stages during this process.

Etiology

Infectious Causes

Reactive lymphocytosis is frequently induced by viral infections, particularly those with lymphotropic properties that directly infect lymphoid cells, prompting an immune response characterized by proliferation of activated T and B lymphocytes. Epstein-Barr virus (EBV) infection, causing infectious mononucleosis, is a classic example, where atypical lymphocytes known as Downey cells—large, activated CD8+ T cells—appear in the peripheral blood, often comprising 10-20% of leukocytes during the acute phase. Cytomegalovirus (CMV) similarly triggers a mononucleosis-like syndrome with atypical lymphocytosis, primarily involving activated CD8+ T cells responding to infected cells. Human immunodeficiency virus (HIV), especially in primary infection, leads to reactive lymphocytosis through direct tropism for CD4+ T cells, resulting in polyclonal activation of both T and B lymphocytes. Hepatitis viruses, such as hepatitis A, B, and C, can also elicit reactive lymphocytosis via lymphotropic effects, with acute infections stimulating atypical lymphocyte expansion as part of the antiviral response. Bacterial infections contribute to reactive lymphocytosis through toxin-mediated or post-infectious mechanisms that disrupt lymphocyte trafficking or cause rebound proliferation after initial suppression. , the agent of , induces marked absolute (often >40,000/μL) via , which inhibits receptors and prevents migration into tissues, leading to accumulation in the blood. , caused by , leads to reactive through chronic antigenic stimulation and granulomatous inflammation. , causing , typically presents with relative during the recovery phase, reflecting a post-infectious rebound as counts normalize and adaptive immunity strengthens against persistent bacterial antigens. Parasitic infections drive reactive lymphocytosis through chronic antigenic stimulation, promoting sustained T-cell activation and . Toxoplasma gondii infection () often manifests as a mononucleosis-like illness with fever, , and peripheral , where reactive lymphocytes respond to intracellular parasite replication in lymphoid tissues. Plasmodium species in , particularly in chronic or hyper-reactive forms, associate with atypical lymphocytosis due to ongoing immune stimulation from parasitized erythrocytes, mimicking viral patterns and occasionally leading to polyclonal B-cell expansion in splenic hyper-reactivity. Severe acute respiratory syndrome coronavirus 2 (), responsible for , exemplifies modern viral induction of reactive lymphocytosis, with atypical lymphocytes observed in approximately 50% of cases, emerging around one week post-symptom onset due to immune dysregulation and cytokine-driven T-cell activation; studies indicate persistent alterations in lymphocyte activation and exhaustion markers in some post-acute cases.

Non-Infectious Causes

Drug reactions represent a significant non-infectious cause of reactive lymphocytes, particularly through syndromes such as drug reaction with and systemic symptoms (DRESS). Aromatic anticonvulsants like and are among the most common culprits, inducing autoimmune-like responses characterized by the proliferation of atypical, reactive lymphocytes alongside and . These reactions often manifest as fever, , and organ involvement, with reactive lymphocytes reflecting T-cell mediated to drug metabolites. Autoimmune diseases, including and systemic lupus erythematosus (SLE), frequently feature reactive lymphocytosis driven by chronic inflammation and dysregulated immune activation. In , reactive lymphoid cells, or immunoblasts, appear in the blood and correlate with disease activity, stemming from persistent antigenic stimulation of T and B . Similarly, in SLE, polyclonal B-cell expansion and autoreactive responses contribute to elevated reactive lymphocyte counts amid ongoing . Various stressors can also provoke reactive , such as acute physiological stress (e.g., epinephrine release from , or excitement), post-transplant immune reconstitution, and responses. Following solid organ or , large granular —a form of reactive expansion—occurs in 5-20% of cases, linked to procedural factors like donor type and post-transplant events including infections or rejection. , including syndromes, elicits transient increases in reactive lymphocytes as part of the adaptive immune activation; for instance, mRNA vaccines have been associated with hypermetabolic lymph nodes on imaging, indicating robust T-cell responses. Other non-infectious triggers include allergic reactions and , which involve immune complex-mediated or T-cell driven leading to reactive lymphocyte proliferation. In -like reactions, often triggered by drugs or vaccines, peripheral blood shows with reactive , reflecting mechanisms. These responses highlight the role of non-pathogenic antigens in stimulating polyclonal activation without microbial involvement.

Clinical Relevance

Diagnostic Significance

Reactive lymphocytes are primarily detected through laboratory evaluation of peripheral blood samples, where (CBC) analysis often reveals , defined as an absolute count exceeding 4,000 cells per microliter in adults. This finding prompts manual review of peripheral blood smears under light microscopy to identify morphological features, such as increased size and irregular nuclei, which distinguish reactive forms from normal . Automated analyzers, such as Sysmex systems, further aid detection by flagging via parameters like RE-LYMP, which measures with elevated intensity compared to the normal population, enhancing efficiency in routine screening. In , the presence of reactive lymphocytes is interpreted within the broader context, including symptoms such as fever and , which commonly accompany underlying infections or immune activations. Serial monitoring of lymphocyte counts via repeat CBCs allows clinicians to assess resolution, as these cells typically decrease following treatment of the inciting condition, guiding decisions on ongoing management without invasive procedures. Prognostically, reactive lymphocytes serve as a benign marker of transient , generally resolving without long-term sequelae once the underlying trigger is addressed. However, in rare cases, persistent or intense activation can contribute to complications like (), a hyperinflammatory triggered by infections and characterized by lymphocyte-mediated tissue damage, necessitating prompt intervention to prevent organ failure. Recent advances in (AI) have improved diagnostic accuracy for reactive lymphocytes, particularly in resource-limited settings where expert microscopists are scarce. For instance, models applied to digital images achieve over 93% accuracy in classifying reactive lymphocytes among various cell types, enabling high-throughput analysis. Automated analyzers like the MC-80, utilizing neural networks for morphological assessment, further support rapid in 2024-2025 clinical workflows, reducing and turnaround times.

Differential Diagnosis

Distinguishing reactive lymphocytes from malignant lymphoid proliferations, such as and , relies primarily on assessing clonality and immunophenotypic profiles. Reactive lymphocytes exhibit polyclonality, as confirmed by demonstrating expression of both kappa and lambda light chains in B cells or diverse rearrangements, whereas leukemic or lymphomatous cells are monoclonal, detectable via (PCR) for (IGH) gene rearrangements or () for chromosomal abnormalities like t(14;18) in . Additionally, reactive lymphocytes lack aberrant immunophenotypic markers typical of malignancies, such as co-expression of CD5 and in (CLL), which is identified in over 90% of CLL cases but absent in reactive processes. Reactive lymphocytes must also be differentiated from blasts in acute leukemias, where morphological overlap can occur, particularly in viral infections producing large, immature-appearing cells. Unlike blasts, which often display fine, dispersed , prominent nucleoli, and occasional in myeloid lineages, reactive lymphocytes typically show coarser , indented nuclei, and abundant basophilic without . Recent advances include analysis, a quantitative technique that evaluates nuclear complexity; a 2025 study demonstrated that models using dimensions achieved 84.2% accuracy in classifying reactive lymphocytes versus blasts, with an area under the curve (AUC) of 0.844, outperforming traditional morphology in ambiguous cases. In contexts of atypical cellular increases, reactive lymphocytosis may coexist with or mimic other reactive changes like or , which share infectious or inflammatory etiologies but differ in and features. Monocytes exhibit kidney-shaped nuclei and gray-blue , while eosinophils display bilobed nuclei and orange-red granules, allowing distinction on smears; however, severe infections can produce concurrent elevations, necessitating lineage-specific counts to avoid conflation. Serial peripheral blood smears are crucial for demonstrating the transient nature of reactive lymphocytosis, which typically resolves within 1-2 months post-stimulation, unlike persistent malignant processes. Diagnostic pitfalls include severe infections mimicking , such as or Epstein-Barr virus mononucleosis, where extreme with blast-like atypia can lead to erroneous bone marrow sampling; for example, in , atypical lymphocytes with associated cytopenias can mimic leukemia, resolving with antibiotics. If persists beyond 3 months or exceeds 5,000/μL without an identified reactive cause, bone marrow is indicated to exclude underlying , providing architectural assessment and confirming polyclonality via additional molecular studies.

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