3. Components of the Autonomic Immune System
In the Cybertronian model, the immune system is a collection of subroutines designed to protect the individual from damage caused by pathogens and foreign materials. In many ways it mirrors the humanoid immune system, particularly in the case of the circulating leukocyte analogues (CLA), self-repairing nanobots found in the circ fluid which are segregated into three categories: detritophagous (dCLA), thrombic (tCLA), and pathocidal (pCLA). The nomenclature here is flawed, as thrombic activity in organic systems is limited to platelets rather than leukocytes, but the circulating nanobots tasked with repairing vessel breaches are indicated as tCLA in order to minimize confusion.
3i. Detritophagous CLA
dCLA are the second most common of the circulating leukocyte analogues, and are responsible for two main functions: firstly, as the name implies, to consume and neutralize any foreign bodies or unnecessary fragments of thrombic material in the circ fluid; secondly, to produce more CLA as required by the immune system as a whole. Given the fact that the dCLA are constantly intaking material at the nanometric level, they are provided with a steady supply of raw material for the construction of new CLA. The entire CLA population is replaced roughly every three Galactic standard months.
Derangements in the dCLA, either structurally or in terms of numbers, can cause several troublesome conditions. If the subroutines that govern production of dCLA are damaged, overproliferation of dCLA (hyperdetritophagemia) can result: these superfluous dCLA then consume the other circulating bodies in the system and lower overall resistance to pathogenic intrusion. In addition, in extreme cases it has been verified that the dCLA begin to consume the actual vessel walls, which can lead to catastrophic structural failure and massive coolant loss. Symptoms of dCLA overproliferation may be slight to negligible until serious damage has been done; therefore, in any case in which dCLA overproliferation is suspected, it is vital to sample the circ fluid and run CLA counts as soon as possible. Waste products from the dCLA nanobotic construction process can also affect the coolant fluid's ability to transfer heat, and may cause the individual to present with a fluctuating overtemp that manifests on a twelve-hour cycle, as the dCLA levels in the circ fluid increase and decrease with the production of new dCLA. The importance of CLA counts in any overtemp condition cannot be overstressed, as this is often the first symptom of dangerous systemic derangement.
Certain conditions, such as contamination of the circ fluid or failure of the pathocidal CLA, can cause underproliferation of dCLA (hypodetritophagemia): this results in a buildup of detritus and chemical imbalances in the circ fluid, as well as an exponential drop in pCLA count, which places the individual at serious risk for pathogenic invasion. Buildup of detritus in the coolant lowers its heat-transfer coefficient and places a strain on secondary heat-transfer mechanisms; this often manifests as a temp control issue, with or without oxygen intake distress, which again should be addressed at once with circ fluid samples and CLA counts.
3ii. Thrombic CLA
The tCLA provide constant internal protection against vessel breach and damage. In the event of accidental or pathogenic vessel breach, the immune subroutines activate tCLA which bind to the edges of the breach and seal it while constructing new myocircuitry to restore the vessel to its original status. They are produced by the dCLA in response to chemical balances in the coolant fluid: a drop in the tCLA chemical signature activates dCLA subroutines to construct additional tCLA. Overproliferation of tCLA (hyperthrombicemia) can cause venous thrombosis and atherosclerosis, generally precipitated by pathogenic derangement of the dCLA which in normal functioning consume and neutralize any excess tCLA. As mentioned above, derangement of dCLA balances is likely to produce systemic power-cooling mismatch conditions manifesting in cyclic overtemp and heat-transfer stress; excess tCLA should be suspected in patients presenting with consistent hypertension and variable overtemp, and counts should be done on all potential hyper-tCLA conditions. Underproliferation of tCLA (hypothrombicemia) places the patient at risk for massive coolant loss with even slight vessel breaching, and any tendency to slow vessel repair and continual coolant loss should be followed up with CLA analysis and counts.
3iii. Pathocidal CLA
The pCLA are often considered the most important of the three subclassifications, as their role is to destroy any foreign or pathogenic intruders within the circ fluid. The immune system records the chemical and physical signature of any pathogen encountered by the pCLA for future reference, and if the pathogen is encountered a second time, the immune response produced by the pCLA will naturally be more rapid and comprehensive given its experience with the pathogenic profile. The science of cybernetic vaccinology is still in its infancy, but studies are underway to determine the viability of vaccines for such pathogens as DHX-1 and Alpha 7; if these studies provide positive results, the potential exists for full eradication of DHX-1 from the galaxy within the next ten years.
Overproliferation of pCLA can be prompted by massive pathogenic or foreign intrusion, as occurs in comprehensive physical damage and vessel breaching: in an otherwise functional individual, this is quickly brought under control as the dCLA engage in reuptake of unnecessary circulatory bodies, but in an immune-compromised individual can quickly spiral into a toxic condition known as hyperpathocidemia. The chemicals produced by the massive numbers of pCLA drastically lower the coolant's heat transfer coefficient, producing severe hyperthermia capable of causing malfunctions in cerebral circuitry: delirium, followed by coma as the cerebral functions trip offline, will occur, and if the hyperpathocidemia is not addressed may proceed further to permanent cerebral damage and deactivation. Hyperpathocidemia must be addressed quickly: emergency treatment consists of total support by external cooling and power lines, deactivation of the pathogen responsible for the initial response, and flushing of the entire coolant circuit to return the CLA balance and chemical composition to nominal. Once this has been accomplished, the immune deficiency or hyperreaction which precipitated the episode of hyperpathocidemia may be addressed. The most important aspect of treating this condition is to maintain cooling to the cerebral circuitry, as heat damage here may not be survivable.
Underproliferation of pCLA (hypopathocidemia) is generally caused by malfunctioning dCLA, and places the individual at risk for massive pathogenic invasion and systemic toxic shock. As the pCLA levels in the circ fluid are not sufficient to mount an appropriate response to the invading pathogen, there is no rapid progression of hyperthermia as in hyperpathocidemia: instead, the effects of the pathogen itself will decrease the efficiency of the coolant fluid and cause a slow but steady rise in temperature and systemic distress. Chemical and thermal imbalances caused by this pathogenic load will manifest themselves in many different subsystems, including the automatic toxin protection system (offloading of fuel from conversion and holding tanks), the gyrostability system (vertigo, disorientation), the oxygen subsidiary cooling circuits (oxygen intake distress), and the neurosensory damage notification system (algesia). As the patient may not be aware of his or her hypopathocidemic condition, these symptoms may come on suddenly, and result in a presentation of multiple systemic failure which can often cause serious psychological distress; for this reason it is important to reassure the patient and attempt to reduce psychological involvement, as this in itself can increase stress-related systemic derangement. Immediate response to the hypopathocidemic patient with a fulminant infection requires total systemic support: sedation via neurocircuitry block may be necessary if the algesia and fuel offloading subroutines go into seizure loops. Matching pCLA should be administered while monitoring vital functions, and a full coolant circuit flush may be necessary to remove the infection completely in cases of very low pCLA production.
Individuals with CLA imbalance should undergo neurocircuitry examination to determine the faulty subroutine in the immune programming which is causing the imbalance, and if necessary undergo total immune reprogramming; this is not desirable, as it places the patient at risk during reprogramming, and constant supportive monitoring must be provided until reprogramming is complete.