Myeloid bias sets the gain on sickness behavior, but the non-classical monocyte signal rests on one cohort

Question: How do myeloid lineage bias and non-classical monocyte expansion relate to sickness behavior and fatigue in inflammatory and oncology populations?

Answer

Read across these papers, myeloid lineage bias is best construed not as a fatigue molecule but as a graded hematopoietic state that raises the gain on sickness behavior, with the non-classical monocyte compartment as its most symptom-specific — and least replicated — readout. The support for bias as a real, quantifiable trait that co-varies with inflammatory burden and functional decline is strong and comes from several independent human datasets [12] [17], and the case that it is durable rather than transient is equally consistent [19]. The support for the stronger claim — that non-classical monocytes specifically generate fatigue — is one breast cancer cohort in which non-classical monocyte abundance tracked sickness-like but not negative-affect symptoms [21]. Meanwhile the animal work locates the fatigue-relevant signal in peripheral-to-interoceptive relay that systemic inflammation engages and selective microglial activation does not reproduce [6] [11]. This survey's position: treat myeloid bias as a validated stratifier and therapeutic entry point, and treat monocyte-subset specificity as a hypothesis that current evidence cannot carry.

Myeloid bias is a graded, ratio-driven state rather than a binary or clone-fixed trait

The extent of myeloid skewing behaves as a quantitative variable with clinical correlates. In humans, a high degree of myeloid skewing was associated with elevated inflammatory markers, reduced mobility, a greater burden of comorbidities, and an increased mortality hazard ratio, while aged mice with more than 50% myeloid cells in blood showed accelerated hematopoietic aging, higher inflammatory cytokines, and impaired HSC repopulation capacity [12].

The mechanism of that bias is contested in a way that matters for whether it can be targeted. Co-transplantation of young and aged long-term HSCs into the same recipients produced nearly equivalent myeloid output, with no myeloid gene enrichment in aged LT-HSCs; instead, reconstituting young HSCs at the aged LT/ST-HSC ratio skewed output to myeloid cells, and aged thymus and spleen independently hindered lymphopoiesis [15].

Myeloid bias also has a state-transition anatomy, not just a ratio. A transient senescent-like population arising from classical CD14++CD16- monocytes drives accumulation of an inflammatory monocyte state in aging humans, orchestrated by AP-1 acting on a pre-established chromatin landscape, and these aged monocytes are transcriptionally primed toward sepsis-associated states [17].

Inflammatory insults convert bias into durable dysfunction, which is what makes it a plausible fatigue substrate

Bias induced by acute injury persists in the progenitor compartment long after the insult resolves. Sepsis survivors showed significant expansion of CD38+ progenitors with increases in granulocyte-monocyte and megakaryocyte-erythroid progenitors, and macrophages differentiated from their HSPCs had downregulated TCA cycle and glycolysis genes plus enhanced type-I IFN and JAK-STAT signalling after LPS stimulation [19]. Prolonged loss of oxidative phosphorylation and mitochondrial mass characterised CD66b+ leukocytes from sepsis patients, persisting for up to six months and linked to adverse clinical outcomes [30].

The same pattern appears where monocyte expansion marks deterioration in inflammatory populations. In cirrhosis, progression to acute-on-chronic liver failure was associated with expansion of classical monocytes, particularly a subcluster with reduced oxidative phosphorylation and marked downregulation of respiratory chain Complex IV genes, validated by respirometry as declining Complex IV-dependent oxygen consumption in pre-ACLF patients [22].

Oncology treatment itself re-engineers the monocyte output. Chemotherapy with cyclophosphamide tilted myelopoiesis toward production of Cxcr4+/Cx3cr1+ neutrophil-like monocytes that suppressed T cells and promoted breast cancer metastasis in mice [18], and in myeloma the marrow imposes metabolic and inflammatory changes that bias hematopoiesis and impair adaptive reconstitution for up to two years post-transplant [31]. Age-associated expansion of bone marrow adipose tissue provides a further route, with leptin-responsive progenitors in yellow marrow driving increased monocyte production and a pro-inflammatory state [14].

The only direct human test of the whole chain finds symptom-domain specificity, not general distress

In 175 women with Stage 0–III breast cancer followed from diagnosis to 18 months post-treatment, greater sickness-like symptom severity was associated with elevated proinflammatory gene expression, Type-I interferon antiviral gene expression, myeloid cell abundance, and particularly non-classical monocytes, whereas negative affect symptoms showed weaker, null, or opposite associations [21]. This is the one paper in the retrieved set that measures myeloid-to-lymphoid and classical-to-non-classical ratios against symptom dimensions in an oncology population, and its discriminating feature is that the association is domain-restricted rather than a global distress effect [21].

Domain restriction is echoed outside oncology. In Long COVID, NLRP3, caspase-1, CRP, IL-18, IL-1β, and gasdermin D were higher in patients who had experienced severe acute infection, and the physio-affective phenome correlated with these immune-inflammatory response system biomarkers [4]. In ME/CFS, mild/moderate and severe groups were discriminated by different cytotoxic and activation phenotypes, with severe patients expressing more IFNγ, TNF, and IL-17 after stimulation [1].

Fatigue-relevant signalling runs from peripheral inflammation to interoceptive cortex, and microglial activation alone does not reproduce it

Selective microglial activation reproduces only part of the sickness repertoire. Chemogenetic microglial activation and endotoxin-driven systemic inflammation both upregulated brain inflammatory genes, reduced voluntary wheel running, and decreased self-care, but only systemic inflammation additionally caused anorexia, weight loss, reduced motivation to work for palatable food, and impaired motor performance [6]. That dissociation places the energetic and motivational components downstream of peripheral immune activation rather than of microglia alone.

The central representation is integrated rather than symptom-by-symptom. Intracerebroventricular prostaglandin E2 produced fever, slower locomotion, quiescence, anorexia, and eye squinting with a distinct activation pattern across the interoceptive network, and insular cortex population dynamics decoded an integrated sickness measure better than individual symptoms [11]. Systemic LPS in female BALB/c mice linked peripheral inflammation and hepatic metabolic and redox changes to region-specific neuronal and microglial responses, hypothermia, reduced food intake, and suppressed locomotion and exploration [3].

Sickness states are also pathogen-specific rather than a single conserved syndrome. Across bacterial, viral, allergic, parasitic, and colitis models, immune challenges elicited unique repertoires of change in behaviour, brain-wide neural activity, and hypothalamic single-cell in situ transcriptomics [8]. In psoriatic disease, inflammation was robustly associated with both depression and fatigue in humans, and inflammatory signalling disrupted thalamostriatal circuitry across species, with thalamus–ventral striatum connectivity correlating with depressive and fatigue-related symptoms [10].

In oncology, myeloid expansion predicts neurological toxicity, and damping the pathway improves function in models but not yet in fatigue trials

Longitudinal profiling after CD19 CAR T cell therapy found expansion of CD163 monocytes and immature CD10lowCD101low neutrophils at peak neurotoxicity, correlating with serum ST2 and IL-2RA and ranking among the strongest predictors of ICANS severity [24]. This is the clearest demonstration in an oncology population that a specific expanded myeloid state tracks a behavioural-neurological syndrome rather than tumour burden.

Interfering with the innate sensing pathway that drives such states reduces fatigue-like behaviour. In an HPV-related head and neck cancer model, tumour growth and chemoradiotherapy activated cGAS-STING with hepatic proinflammatory and metabolic changes, and the STING antagonist H-151 attenuated hepatic inflammatory signatures and mitigated tumour- and treatment-associated reduction in voluntary wheel running [20].

Manipulating lineage balance itself improves physical function, at least in aging. IL-4 inhibited inflammation-induced myelopoiesis and shifted multipotent progenitors toward lymphoid output via an IL-4R–FLT3–STAT6 axis, and long-term IL-4 treatment of aged mice improved immune, metabolic, physical, and cognitive functions, effects recapitulated by transplanting IL-4-treated HSPCs [13]. Conversely, blocking IL-10R prolonged HSC cycling after inflammation and accelerated aging hallmarks including myeloid bias [16].

Human causal evidence that lowering inflammation changes effortful behaviour exists but is not in oncology and not about fatigue as such: in a randomised placebo-controlled trial in obesity, colchicine decreased systemic inflammation, increased high-effort food choices, and marginally decreased effort-related dorsomedial prefrontal signal [26]. For fatigue itself, the interventional evidence base is thin — a systematic review of low-dose naltrexone in long COVID found no randomised controlled trials and only four pre-post studies, with low certainty [9].

Conflicts and gaps

The inflammatory signal in fatigue syndromes is not reliably reproducible. A primary-care long COVID cohort showed no evidence of elevated CRP, TNF, IL-1β, or IL-6 [27], and a separate characterisation found no obvious deviation in monocyte profiles in long COVID, with the major changes in CD4+ T cell exhaustion, regulation, and differentiation [23]. Against this, multi-omics in ME/CFS reported an exaggerated innate immune response to microbial stimulation, systemic inflammation linked to lipid abnormalities, and worsening after exercise [7], while direct monocyte and dendritic cell immunophenotyping in 207 participants found increased M2-like monocyte polarisation and CD80 expression in long COVID versus reduced costimulatory expression and impaired CCR7 trafficking in ME/CFS [2]. Case definition, sampling interval, and assay sensitivity differ across all of these.

Which monocyte subset is the operative one is unresolved. Non-classical monocytes carry the symptom association in breast cancer survivors [21], but classical monocyte expansion marks deterioration in cirrhosis [22], classical CD14++CD16- cells are the source of the age-associated inflammatory state [17], and CD163+ monocytes mark CAR T neurotoxicity [24]. Part of this may be measurement: a TLR2pos CD14dim/neg CD16neg population previously read as monocyte was found to comprise largely CD163pos CD1cpos dendritic cells, and gating strategy materially changed population composition [25].

Whether bias causes fatigue, or illness behaviour and inactivity cause bias, is not addressed by any retrieved study; all human evidence is observational and cross-sectional or longitudinal-associational. Scepticism is warranted more broadly: in a heterogeneous adult sample, provoked pro-inflammatory cytokine expression was not associated with childhood adversity, induced secondary hyperalgesia, or vaccine-associated change in conditioned pain modulation [5].

What would change the answer

Subset-specific causation needs a perturbation, not another correlation. The decisive experiment is selective depletion or blockade of non-classical monocytes (anti-CX3CR1 or CCR2-axis strategies) in a tumour-bearing or chronic-inflammation model with objective fatigue endpoints — voluntary wheel running, effort-based operant responding, and actigraphy — benchmarked against the dissociation already established between microglial and systemic routes [6]. Reversing bias upstream with IL-4R–FLT3–STAT6 agonism while measuring physical function would test whether lineage balance is causal rather than an epiphenomenon [13].

Human temporal precedence requires dense longitudinal sampling with baseline pre-treatment immune profiling and repeated symptom dimensions, extending the breast cancer design beyond five time points and adding mediation analysis against inflammatory and Type-I IFN gene expression [21]. Clonal haematopoiesis offers a natural experiment in myeloid bias: carriers can be followed prospectively for fatigue and functional trajectories, building on the observation that clonal haematopoiesis, a marker of systemic immune activation, trended toward improved survival in liver cancer [29].

A safe human inflammatory challenge model using interferon-β, designed to elicit sickness responses within hours with minimal cardiovascular effects and usable across the age range [28], would allow pre-challenge monocyte subset frequencies and classical-to-non-classical ratios to be tested as predictors of sickness-response magnitude. Pairing that with standardised, gating-robust subset definitions [25] and with anti-inflammatory or STING/NLRP3 blockade arms using symptom-domain-specific endpoints [26] [20] would convert the current associational picture into a testable causal chain.

References

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How this survey was made

This survey answers one question: “How do myeloid lineage bias and non-classical monocyte expansion relate to sickness behavior and fatigue in inflammatory and oncology populations?”

We keep our own collection of recent preprints and refresh it every day from bioRxiv, medRxiv, arXiv, PsyArXiv, SocArXiv and ChemRxiv. For each survey, we search that collection for recent work and keep the strongest matches: papers that use the same terms as the question, and papers on the same topic in different words.

The text was written from the titles and abstracts of those papers; the full texts were not read. Statements that draw on a particular paper are marked with a number in brackets. The reference list just above is the 31 papers whose work this text draws on, chosen from the 127 papers those searches returned; the rest of the shortlist is not printed. It is not a complete review of everything published on the question.

Treat this as a starting point and a reading list, not a peer-reviewed review. The searches behind this survey ran on October 22, 2026 and covered work from the previous two years.